From a pathophysiological point of view, bronchiectasis disease is sustained by a vicious circle in which an alteration in mucociliary clearance is followed by chronic respiratory infections, chronic inflammation, and irreversible bronchial anatomical damage, which over time can lead to a progression and aggravation of the disease itself.

 What are the causes of bronchiectasis?

Bronchiectasis can have several causes, either congenital or acquired, such as primary or secondary immune deficits, previous pneumonias, alterations in ciliary motility, fungal infections (such as from Aspergillus) or from non-tuberculous mycobacteria, autoimmune and chronic inflammatory processes.

However, in 40-50% of cases the cause of the disease remains unknown despite extensive diagnostic investigations.

What are the symptoms of bronchiectasis?

The main symptoms/signs of bronchiectasis are coughing, daily expectoration, and recurrent respiratory infections (including pneumonia).

In addition to these symptoms, episodes of haemophthisis/haemoptysis (blood in the sputum), dyspnoea (shortness of breath), persistent fever, and daily significant asthenia may also be present.

Diagnosis

The gold standard for the diagnosis of bronchiectasis is a high-resolution chest CT scan and the pulmonologist is the referral specialist.

At the time of the diagnosis of bronchiectasis and depending on the severity of the clinical picture, a series of laboratory tests should be performed, including quantitative assessment of total IgG, IgA, IgM and IgE immunoglobulins, IgG and IgE specific for A. fumigatus, protein electrophoresis, complete respiratory function tests, a sputum culture test for bacteria, fungi and mycobacteria, a visit with a respiratory physiotherapist and a pulmonologist.

Then, every six months or annually, and always depending on the severity of the clinical picture, it is recommended to perform a sputum culture examination, and a re-evaluation with a respiratory physiotherapist and a pulmonologist.

In some patients it is also important to rule out certain genetic disorders (such as cystic fibrosis or primitive ciliary dyskinesia) as well as the coexistence of possible connective tissue diseases (such as rheumatoid arthritis).

Treatments

There are to date no European or American approved drugs to treat this disease.

The management of bronchiectasis is totally individualised on the basis of the clinical and biological characteristics expressed by each patient.

The most important treatment is respiratory physiotherapy, which uses a specific exercise programme to remove the mucus that tends to stagnate in bronchiectasis.

Other important tools at our disposal are antibiotics, immunomodulatory therapies, bronchodilator drugs (if bronchial obstruction is present) as well as treatments to manage the two most frequent complications of the disease: flare-ups and the presence of blood in the sputum.

The optimal management of bronchiectasis passes through a multidisciplinary approach in which the pulmonologist, flanked by the respiratory physiotherapist, can count on the collaboration of other professionals including the clinical microbiologist, the radiologist, the clinical immunologist/rheumatologist, the geneticist, the gastroenterologist and the otorhinolaryngologist.

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A Guide To Chronic Obstructive Pulmonary Disease COPD

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Mucus in the lungs is common in certain health conditions and needs treatment. For example, if you have bronchiectasis or chronic obstructive pulmonary disease (COPD), clearing mucus from your lungs is an important part of managing your lung disease.

Having too much mucus in your lungs or phlegm build-up can block narrowed air passages and make it hard for you to breathe. Increased mucus in the lungs can also lead to infections, such as pneumonia.

There are ways to treat mucus in the lungs, including controlled coughing, medications, and chest physiotherapy.

This article will go over some causes of mucus in the lungs as well as ways that your provider might want you to clear mucus from your lungs as part of your treatment.

Verywell / Emily Roberts

Home Remedies and Lifestyle Changes for Mucus in Lungs

You can use at-home exercises to help prevent and decrease mucus buildup in your lungs. If you have lung disease these techniques should be used regularly to loosen and remove the excess mucus from your lungs.

Controlled Coughing for Mucus in Lungs

Controlled coughing engages the chest and stomach muscles to clear mucus in the lungs. Unlike a hacking cough that uses the chest muscles more than the diaphragm, controlled coughing focuses on stabilizing the core muscles to engage the diaphragm more effectively.

There are two common methods of controlled coughing: deep and huff.

How to use deep coughing to clear mucus in the lungs:

  1. Sit comfortably in a chair with your feet on the ground.
  2. Wrap your arms around your stomach, and take a deep breath in.
  3. Keeping your lips pursed, cough forcefully while pressing your arms firmly against your stomach muscles.

How to use huff coughing to clear mucus in the lungs:

  1. Take a deep, slow breath to fully expand your lungs.
  2. Tense your stomach muscles
  3. Exhale three times very quickly and make a "ha" sound with each breath.
  4. Repeat this step, keeping your core firm, until you feel the mucus in your lungs breaking up.
  5. Cough deeply to clear your lungs.

Deep Breathing for Mucus in Lungs

When you do deep breathing exercises, you slowly breathe in (inhale) and breathe out (exhale) to help your lungs expand. These breathing exercises are examples of pulmonary hygiene—treatments that use physical manipulation techniques to help you cough up sticky mucus and clear your lungs.

Your respiratory therapist can teach you deep breathing techniques that you can do at home on a regular schedule to help keep your lungs clear.

Over-the-Counter (OTC) Treatment for Lung Mucus

Several OTC medications can help clear excess mucus from your lungs, for example, Robitussin and Mucinex.

These medications are expectorants. They have an ingredient called guaifenesin in them that thins and loosens mucus in the lungs to make it easier to cough up. They can also block the production of the main protein in mucus (mucins).

Most expectorants can be bought at a pharmacy or grocery store, but some combination drugs that have expectorants and other ingredients in them require a healthcare provider's prescription.

Prescription Medications for Lung Mucus

Mucolytics, including N-acetylcysteine and carbocysteine, are only available by prescription.

These medications work differently than expectorants. Mucolytics break the chemical bonds in mucus to help make it easier to cough up.

Chest Physiotherapy for Mucus in Lungs

Chest physiotherapy (CPT) techniques can be done manually or with a mechanical device. A CPT routine can take anywhere from 20 minutes to an hour.

You can do some CPT techniques by yourself, but others require help from a partner, such as a therapist or a family member at home.

  • Manual CPT combines chest percussion and vibration to loosen the mucus in the lungs and make you cough. To do chest percussion, a therapist or loved one will clap on your chest or back to help loosen the thick mucus in your lungs so you can cough it up. Vibration is done by placing their flat hands on your chest wall and making a shaking motion.
  • Airway clearance devices are hand-held machines that use high-frequency vibration, low-frequency sound waves, and other technology to break up mucus in the lungs. They are easy to use by yourself. Some of the devices are worn like a vest, while others require you to breathe into them (like a flute).

While you are having chest physiotherapy, make sure you breathe in and out slowly and fully until the mucus in your lungs is loose enough to cough up. Your therapist will show you how to get into a position that uses gravity to help the mucus in your lungs drain.

Alternative Medicine for Lung Mucus

There are some natural remedies that may help reduce the mucus in your lungs. Keep in mind that even though they are "natural," complementary and alternative medicine (CAM) therapies can have side effects.

CAM therapies that may help clear mucus in the lungs include:

  • Warm fluids: Drinking warm (not hot) liquids can help loosen thickened mucus. Try tea, warm broth, or hot water with lemon.
  • Steam: You can use a device such as a cool-mist humidifier or steam vaporizer to breathe in warm air. You can also take a hot shower or breathe in vapors from a pot of simmering water. These methods introduce moist air into your air passages, which helps loosen the mucus in your lungs. However, do not inhale oils because they can cause an inflammatory or allergic lung reaction.
  • HoneyHoney may reduce inflammation and coughing. However, it is not clear whether honey specifically helps in coughing up mucus.
  • Chinese medicine: Chinese herbs and treatments have traditionally been used to reduce mucus in the lungs. While there are anecdotal reports that they are helpful, the scientific data is not clear about the benefits.
  • A few herbs—including mao huang (Herba ephedrae), tao ren (Semen persicae), and Huang qin (Radix scutellariae)—may ease the symptoms of respiratory disease.
  • Qigong, a practice of breathing exercises and movements, may also help.

Ask Your Provider About CAM for Lung Mucus

CAM therapies are not safe for everyone. If you take certain medications or have certain health conditions, you may not be able to use them.

If you want to try an herb, supplement, or natural remedy to help clear mucus in your lungs, talk to your provider. They will make sure that it would be safe for you to try these treatments.

Summary

Mucus in the lungs can be part of having certain health conditions and something that you'll need to learn how to manage.

Regularly clearing mucus from your lungs is part of living with bronchiectasis and COPD. Controlled coughing, deep breathing, over-the-counter and prescription medications, chest physiotherapy, and alternative therapies help by reducing, loosening, and coughing up the mucus to prevent lung infections.

It's important that you use mucus-reducing strategies on a regular basis, not just when your symptoms act up. If you have been diagnosed with pulmonary disease, talk to your healthcare provider or respiratory therapist about the best approaches for managing mucus in your lungs.

Frequently Asked Questions

  • How do you know if your lungs are filled with mucus?

    If you have mucus in your lungs, you might have a "wet" cough or be able to hear the fluid in your chest when you breathe. You may wheeze or find it harder to breathe if there is mucus build-up in your lungs.

  • How do I naturally get rid of mucus in the lungs?

    One way to get rid of mucus or phlegm naturally is by doing controlled huff coughing to clear your lungs.

    1. Sit up straight, slightly tilt your chin toward the ceiling, and open your mouth.
    2. Slowly take a deep breath in, filling your lungs about three-quarters full.
    3. Hold your breath for three seconds.
    4. Forcefully exhale in a slow, continuous manner.
    5. Repeat steps one to four at least two or three more times. Then, perform a single strong cough. This should remove mucus concentrated in the larger airways.

  • Is chest congestion common in COVID-19?

    About one-third of people with COVID-19 have chest congestion or pressure as a symptom. COVID often causes a dry (non-productive) cough but some people have a productive cough and cough up thick mucus.

  • What causes phlegm?

    The body makes phlegm and mucus to line the tissues and protect and moisturize them, as well as trap potential irritants and germs.

  • What medicine can be used to clear phlegm from the throat?

    Mucus thinners (mucolytics) are over-the-counter (OTC) medicines that help thin mucus or phlegm in the airways, making it easier to cough up. Two types of mucus thinners are Pulmozyme (dornase alfa) and hypertonic saline.

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
  1. Poole P, Sathananthan K, Fortescue R. Mucolytic agents versus placebo for chronic bronchitis or chronic obstructive pulmonary disease. Cochrane Airways Group, ed. Cochrane Database of Systematic Reviews. 2019 May 20;5(5):CD001287. doi:10.1002/14651858.CD001287.pub6

  2. Aaron SD. Mucolytics for COPD: negotiating a slippery slope towards proof of efficacy. Eur Respir J. 2017;50(4). doi:10.1183/13993003.01465-2017

  3. Warnock L, Gates A. Chest physiotherapy compared to no chest physiotherapy for cystic fibrosis. Cochrane Database Syst Rev. 2015;(12):CD001401. doi:10.1002/14651858.CD001401.pub3

  4. Cohen HA, Hoshen M, Gur S, Bahir A, Laks Y, Blau H. Efficacy and tolerability of a polysaccharide-resin-honey based cough syrup as compared to carbocysteine syrup for children with colds: a randomized, single-blinded, multicenter studyWorld J Pediatr. 2017;13(1):27-33. doi:10.1007/s12519-016-0048-4

  5. Tong H, Liu Y, Zhu Y, Zhang B, Hu J. The therapeutic effects of qigong in patients with chronic obstructive pulmonary disease in the stable stage: a meta-analysis. BMC Complement Altern Med. 2019;19(1):239. doi:10.1186/s12906-019-2639-9

  6. American Lung Association. Understanding Mucus in Your Lungs.

  7. Centers for Respiratory Health. Clearing lung mucus in five easy steps with huff coughing.

  8. Cystic Fibrosis Foundation. Mucus thinners.

By Deborah Leader, RN

 Deborah Leader RN, PHN, is a registered nurse and medical writer who focuses on COPD.

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Chronic Obstructive Pulmonary Disease is a broad term used for defining progressive lung diseases like emphysema, refractory asthma, chronic bronchitis and some other forms of bronchiectasis. The symptoms of Chronic Obstructive Pulmonary Disease are so common that sometimes people fail to understand that they are suffering from Chronic Obstructive Pulmonary Disease and consider it as normal cold, cough and symptoms of aging. Symptoms are sometimes not even visible in the early stages of disease and the disease remains undiagnosed for a long time.

The symptoms of Chronic Obstructive Pulmonary Disease include wheezing, tightness in the chest, frequent coughing and increased breathlessness. Chronic Obstructive Pulmonary Disease can be treated using different types of drugs and therapies including oxygen therapy and pulmonary rehabilitation programs. In case of extreme severity of Chronic Obstructive Pulmonary Disease surgery is recommended which includes lung volume reduction surgery, lung transplant and bullectomy.

According to the data of British Lung Foundation approximately 1.2 billion people were suffering from Chronic Obstructive Pulmonary Disease in the U.K. alone in 2011. Also according to the COPD Foundation approximately 30million Americans were suffering from Chronic Obstructive Pulmonary Disease in 2013. Chronic Obstructive Pulmonary Disease is one of the leading causes of death worldwide. This data demonstrates the ever increasing demand of Chronic Obstructive Pulmonary Disease treatment worldwide and hence also shows the potential that the Chronic Obstructive Pulmonary Disease therapeutics market holds.

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Chronic Obstructive Pulmonary Disease Therapeutics Market: Drivers and Restraints

The most important factors that are expected to drive the growth of the Chronic Obstructive Pulmonary Disease market includes the ever increasing number of cases of Chronic Obstructive Pulmonary Disease globally. Also the change in the lifestyle is responsible for increasing the habits like smoking and increase in the number of genetic disorders which in turn are responsible for raising the number of Chronic Obstructive Pulmonary Disease patients.

Other factors that can boost the revenue from the Chronic Obstructive Pulmonary Disease therapeutics market are rising expenditures on healthcare that is leading to the adoption of Chronic Obstructive Pulmonary Disease treatments in the emerging economies. Increase in the level of awareness has also lead to the early diagnosis of the Chronic Obstructive Pulmonary Disease so that people can go for the treatment of the disease.

Factors that can limit the growth of the therapeutic enzymes in the forecast period include the fact that not all the patients who are suffering from Chronic Obstructive Pulmonary Disease are aware of the fact that they are suffering from the disease and therefore do not go for the treatment of the disease. Also sometimes people get to know about their disease when the disease can’t be cured by only medication and therapies and surgery becomes mandatory. This factor can also lead to a slow growth in the revenue from the Chronic Obstructive Pulmonary Disease therapeutics market.

Chronic Obstructive Pulmonary Disease Therapeutics Market: Overview

Chronic Obstructive Pulmonary Disease therapeutics market is a growing market and is expected to see an even higher growth in the forecast period. Factors such as increase in the population suffering from Chronic Obstructive Pulmonary Disease worldwide and increasing awareness about Chronic Obstructive Pulmonary Disease are responsible for fueling the growth of the Chronic Obstructive Pulmonary Disease therapeutics market.

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Betterment of the healthcare infrastructure in Asia Pacific and Middle East and Africa is also responsible for the revenue growth of the Chronic Obstructive Pulmonary Disease therapeutics market in the forecast period.

Chronic Obstructive Pulmonary Disease Therapeutics Market: Region-wise Outlook

Chronic Obstructive Pulmonary Disease therapeutics market is in its growth phase and hence this market is expected to see very high growth in the emerging economies like Latin America and Asia Pacific due to high population growth in these regions. North America Chronic Obstructive Pulmonary Disease therapeutics market is the most developed market in terms of revenue, followed by Europe. Middle East and Africa are also expected to see higher growth due to growing advancement in the healthcare infrastructure.

Chronic Obstructive Pulmonary Disease Therapeutics Market: Key Market Participants

Some of the key participants of Chronic Obstructive Pulmonary Disease therapeutics market include Pfizer Inc, Adamis Laboratories Inc., GlaxoSmithKline plc.

The report covers exhaustive analysis on

  • Market Segments
  • Market Dynamics
  • Historical Actual Market Size, 2012 – 2014
  • Market Size & Forecast 2017 to 2027
  • Supply & Demand Value Chain
  • Market Current Trends/Issues/Challenges
  • Competition & Companies involved
  • Technology
  • Value Chain
  • Aircraft Refurbishing Market Drivers and Restraints

Regional analysis includes

  • North America
  • Latin America
  • Europe
  • Asia Pacific
  • Middle East & Africa

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The report is a compilation of first-hand information, qualitative and quantitative assessment by industry analysts, inputs from industry experts and industry participants across the value chain. The report provides in-depth analysis of parent market trends, macro-economic indicators and governing factors along with market attractiveness as per segments. The report also maps the qualitative impact of various market factors on market segments and geographies.

Chronic Obstructive Pulmonary Disease Therapeutics Market: Segmentation

Chronic Obstructive Pulmonary Disease Therapeutics Market: Segmentation

Chronic Obstructive Pulmonary Disease therapeutics market can be segmented on the basis of components and end user.

On the basis of component

  • Drug Class
  • Bronchodilators
  • Steroids
  • Phosphodiesterase-4 inhibitors
  • Theophylline
  • Antibiotics
  • Delivery Systems
  • Oral
  • Inhalation

On the basis of end user

  • Hospitals
  • Private clinics
  • Out-patients

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Future Market Insights (ESOMAR certified market research organization and a member of Greater New York Chamber of Commerce) provides in-depth insights into governing factors elevating the demand in the market. It discloses opportunities that will favor the market growth in various segments on the basis of Source, Application, Sales Channel and End Use over the next 10-years.

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Empyema is the accumulation of pus in the pleural cavity which can be linked to lung abscesses, trauma, septicemia, or spinal osteomyelitis. It is usually caused by a lung infection that extends to the pleural space and causes pus to accumulate. Here, we present the case of a 70-year-old male who complained of dry cough for 15 days, breathlessness on walking for 20 days, right-sided chest and upper back pain, and high-grade fever for 15 days. On investigation, pleural empyema was diagnosed. He underwent a thoracoscopy to drain the fluid and an intercostal drainage tube was inserted. Along with medical management, physiotherapy was also required to help the patient to perform his daily activities with ease. A physiotherapy protocol was developed for the patient to improve his condition.

Introduction

Pleural empyema is a serious infection-related complication that rarely resolves without appropriate medical therapy and drainage procedures. Empyema is the accumulation of pus in the pleural cavity which can be linked to lung abscesses, trauma, septicemia, or spinal osteomyelitis. It is usually caused by a lung infection that extends to the pleural space and causes pus accumulation [1]. Clinical signs include persistent fever and pleural involvement. Tuberculosis is also one of the causes of pleural empyema usually in the elderly as immunity decreases with age and other degenerative processes in the body begin to occur [2]. On the other hand, empyema can also be a secondary cause of pleural effusion. Pleural effusion is an excessive accumulation of fluid in the pleural cavity. It can be secondary to pneumonia, tuberculosis, malignancy of the lungs, lung abscess, lymph node blockage, and many more diseases. Usually, patients have dyspnea, cyanosis if the effusion is large, pain, lethargy, and restricted thoracic movements [3]. The pleural layers come together and may become adherent leading to the organization of fibrin due to the presence of plasma proteins in the fluid. The presence of fibrous tissue leads to restricted lung mobility, eventually causing alteration in the breathing pattern of the patient [4]. Patients require multidisciplinary treatment. Along with medications, physiotherapy also plays a crucial role in the treatment protocol for pleural effusion as well as in pleural empyema. The aim of physiotherapy is to avoid the formation of disabling adhesions between two pleura layers, regain full lung expansion, improve the ventilation of the lungs, improve the exercise tolerance capacity, and maintain joint mobility [3,4]. In this case, the patient was diagnosed with pleural empyema post-pleural effusion a few months ago and was undergoing treatment and rehabilitation for improvement in his condition. He was referred to the physiotherapy department where a proper well-planned treatment protocol was developed for the patient.

Case Presentation

A 72-year-old male, farmer by occupation, came to the hospital with complaints of dry cough, breathlessness on walking, right-sided chest pain and upper back pain for 15 days, and high-grade fever for 15 days. The pain progressed gradually. The patient also provided a history of low-grade fever for two days. After the development of these symptoms, he was taken to a private hospital near his residence where medications were prescribed. The patient was a chronic bidi smoker for 30 years, smoking three to four bidis per day. In the hospital, he underwent computed tomography (CT) scan of the thorax and was advised a thoracoscopy. During the procedure, 100 mL of thick pus was aspirated through thoracoscopy. Post-thoracoscopy, when the patient was stable, a clinical examination was done. He was in supine lying position, conscious, and well-oriented to time, place, and person with a mesomorphic build. During observation, a Foley catheter and an intercostal drainage tube (ICD) number 28 were present, and chest movements were decreased. On examination, pulse rate was 104 beats/minute, blood pressure was 130/88 mmHg, and oxygen saturation was 98%. His breathing pattern was abdomino-thoracic type with a respiratory rate of 23 breaths/minute. On palpation, the chest was asymmetrical, chest expansion was decreased, and the trachea had shifted to the left side. Stony dullnote and decreased vocal resonance over the right side were noted when percussed. The air entry was reduced on both sides, although more on the right. The patient was suspected for tubercular pleural empyema. Therefore, he underwent a high-resolution CT (HRCT) scan of the lungs on January 22, 2022. It revealed moderate right pleural effusion with loculations in places. Consolidation with sub-segmental compression atelectasis was seen in the underlying right lower and middle lobe region. Again, HRCT of the lung was done on January 27, 2022, which revealed, small air foci in the pleural collection, post-tapping status. Small patchy pneumonitis areas in both upper lobes were noted, suggestive of infectious etiology. The radiographical findings are shown in Figure 1. Later, 400 mL of pleural fluid was sent for cytopathological examination. It was reddish hemorrhagic fluid and suggested acute inflammatory leucocytic suppurative exudation like empyema. A high-dose contrast-enhanced computed tomography (CECT) scan of the thorax was done, which revealed a peripherally enhancing loculated large pleural collection noted on the right side causing the collapse of the right lung plus mediastinal shift and multiple enhancing lymph nodes, suggestive of empyema and right lung collapse. Other lab investigations were done; on complete blood count testing, the haemoglobin was reduced (10.9 g/dL). The kidney function test showed a reduced sodium level (128 mEq/L) and reduced creatinine level (0.6 mg/dL).

Therapeutic intervention

The objective of physiotherapy was to enable him to return to his everyday activities and health maintenance. The detailed physiotherapy rehabilitation protocol is presented in Table 1.

Goals Therapeutic interventions Treatment protocol
Patient education Educating the patient about exercises and its importance. Gaining cooperation and consent from the patient and his family The patient and the caregiver were educated about the importance of positioning, ambulation, and functional activities of daily living
To improve bed mobility Monitored for bed transitions and bedside sitting Patient was taught rolling and bedside sitting. Positioning helped prevent bed sores, facilitate drainage, and improve ventilation which increased oxygen uptake
To retrain breathing pattern and reduce dyspnea Controlled breathing exercises were taught, which included, pursed lip breathing and diaphragmatic breathing The patient was advised to perform these exercises 10 times two to three times a day which improved the breathing efficiency
To improve lung volume Thoracic expansion exercises, flexion of shoulder with deep inspiration, and expiration while extension Ten repetitions in one set twice a day were prescribed
Active range of motion exercises for the upper and lower limbs Range of motion exercises for all joints of the upper and lower limbs Daily 8-10 repetitions for each joint actively. This maintained the joint mobility
To improve lung volume and capacity Thoracic expansion exercises: shoulder in flexion with deep inspiration and extension with expiration. Incentive spirometer was used. Visual feedback through differently colored balls representing 600, 900, and 1200 cc Initially 10 repetitions in one set twice a day; later, 10 repetitions in two sets three to four times a day. Initially, the patient was told to perform spirometry two to three times a day; later, the patient was suggested to perform spirometry every two hours
Early mobilization Ambulation in the hallway Early mobilization helps in improving the functional residual capacity

Follow-up and outcome measures

Table 2 presents the detailed follow-up and outcome measures of the patient.

Outcomes First day of referral At the time of discharge Follow-up
Grades of dyspnea II I I
St. George’s Respiratory Questionnaire 76 58 55
Hospital Anxiety and Depression Scale 10 6 5

Discussion

Empyema is the collection of pus in the pleural cavity most commonly caused by pre-existing lung diseases such as bacterial pneumonia, tuberculosis, lung abscess, or bronchiectasis. Direct infection into the pleural space is the most common cause [5]. Clinical signs include continuing fever with signs of pleural involvement. The goals of the treatment are to eliminate the infection, obtain full lung expansion, and prevent the development of a rigid chest wall. Pleural aspiration, instillation of antibiotics, and physiotherapy are the daily treatment plan for patients [3]. Pleural effusion occurs when fluid settles in the pleural cavity. It can occur by transudation or exudation. It may be asymptomatic or associated with pleuritic pain [6]. Empyema can be a secondary cause of pleural effusion. When patients experience such conditions, a physiotherapist can assist in regaining mobility and function and improving their quality of life [7]. Chest physiotherapy has long been a standard aspect of treatment after a thoracoscopy [8] and includes patient education, early mobilization, splinted coughing or huffing, thoracic expansion exercises, using mechanical devices, and well-planned home exercise program during discharge [7,9]. We can conclude that flow-metric incentive spirometry, combined with breathing exercises and airway clearing techniques, can be effective in improving pulmonary function, forced vital capacity, and functional capacity. Chest physiotherapy has an essential role in both preventing and treating pulmonary problems.

Conclusions

It has been demonstrated that pulmonary rehabilitation improves patient ventilation and reduces dyspnea. It helps in the faster recovery of patients. In this case, after the rehabilitation, the patient was able to perform functional activities independently without feeling exhausted. The breathlessness was also reduced post-rehabilitation. Even though complete recovery was not achieved following rehabilitation, the patient’s lung vital capacity and exercise tolerance were significantly improved.



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Bronchiectasis is a lung condition that causes a persistent cough and excess phlegm, or sputum. It is a permanent condition that gets worse over time. It can be fatal.

The bronchi dilate, usually irreversibly, and phlegm builds up. This leads to recurrent lung infections and lung damage.

It can affect people with tuberculosis and cystic fibrosis, but these are not the only causes. Various processes and mechanisms can trigger this disorder.

There is no cure, but treatment can reduce infections and mucus build up. Symptoms vary in severity.

Older age increases the risk of, but bronchiectasis can affect all ages. In the United States (U.S.), it affects about 25 people in every 100,000. Over the age of 74 years, this increases to about 272 cases per 100,000 people.

The prevalence appears to be increasing.

Symptoms are thought to start when sputum builds up in the respiratory system, leading to a cycle of problems.

More sputum means more bacteria in the airways, and this leads to inflammation and airway destruction. Then the cycle begins again with more mucus.

There are three main types of bronchiectasis, classified according to the resulting shape of the bronchi, visible on a CT scan of the lungs.

They are:

  • Cylindrical: The most common form, with even, cylinder-shaped bronchi
  • Varicose: The least common form. Bronchi are irregular, and the airways may be wide or constricted, leading to a higher production of sputum.
  • Cystic: Almost as common as cylindrical, but the bronchi form clusters of cysts. This is the most severe form.

The different types have similar symptoms are similar across the different types, but they differ in terms of severity.

They all feature enlargement of the breathing tubes of the lungs, or bronchi.

Other symptoms include:

  • a daily cough that continues for months or years
  • daily production of sputum in large amounts
  • shortness of breath and wheezing when breathing
  • chest pain
  • coughing up blood

A person with bronchiectasis who then gets an infection can experience a flare-up, and this can worsen the lung function.

In time, flares and infections can lead to complications.

Respiratory failure

When too little oxygen transfers from the lungs into the blood, or too little carbon dioxide, a waste gas, is removed from the blood, respiratory failure can occur.

Symptoms include:

  • shortness of breath
  • rapid breathing
  • air hunger, or the constant need for more air
  • sleepiness
  • bluish skin, fingernails, and lips

Atelectasis

Atelectasis happens when at least one area of the lung fails to inflate properly, leading to shortness of breath, rapid breathing and heart rate, and bluish lips and skin.

Heart failure

At the most advanced stages of bronchiectasis, lung function worsens, putting a strain on the heart. The heart can no longer pump enough blood to meet the body’s needs.

The person may experience:

  • trouble breathing
  • tiredness
  • swelling of the abdomen, neck veins, feet, ankles, and legs

Untreated, it can be fatal.

Bronchiectasis occurs when a part of the bronchial tree widens irreversibly or dilates.

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Excess mucus encourages bacteria to thrive, leading to damage in the airways.

A wide range of factors can lead to it, including some congenital and autoinflammatory conditions and infections.

Infections that have been linked to bronchiectasis include:

Immunodeficiency conditions include:

It has also been linked to:

  • allergic bronchopulmonary aspergillosis
  • obstruction by a tumor or a foreign body
  • gastro-esophageal reflux
  • inhaling toxic fumes
  • auto-inflammatory conditions, such as rheumatoid arthritis, lupus, and ulcerative colitis, or Crohn’s disease
  • cystic fibrosis and some other congenital conditions

Between one third and one half of patients appear to have no identifiable cause.

Cystic fibrosis (CF) is a common cause of bronchiectasis in children. This is called CF bronchiectasis. Non-CF bronchiectasis is when the person has bronchiectasis but not CF.

Between 7 and 25 percent of patients with asthma or chronic obstructive pulmonary disease (COPD) also have bronchiectasis, but how these related to bronchiectasis remains unclear.

How does bronchiectasis affect the lungs?

Air passages in the respiratory system make it possible for oxygen to enter the lungs and for carbon dioxide to leave the body.

In healthy lungs, the bronchial tubes narrow smoothly towards the edges of each lung, but in bronchiectasis, they widen and become collapsible and scarred.

The cilia, the hair-like structures that sweep mucus out of the lungs, no longer function ineffective, so the mucus builds up.

This increased mucus provides a place for bacteria to grow. Ongoing infections increase inflammation, and this leads to worsening lung damage.

Is bronchiectasis the same as COPD?

Bronchiectasis, chronic obstructive pulmonary disease (COPD), and cystic fibrosis are classified as obstructive lung diseases.

COPD refers to a collection of lung conditions that make it difficult to breathe, because the airways become inflamed and narrowed. Two conditions that are classified as COPD are persistent bronchitis and emphysema.

Bronchiectasis and COPD are not the same disorder, but studies suggest that between 25 percent and 50 percent of people with COPD also have bronchiectasis.

A person with an ongoing cough, recurrent lung infections, and sputum in the blood may have bronchiectasis.

Tests may include:

  • a chest x-ray
  • a CT scan of the lungs
  • a lung, or pulmonary, function test (PFT)
  • A bronchoscopy, where the doctor uses a lighted tube to look into the lungs, and possibly take a tissue sample

However, laboratory tests do not generally find any specific microorganism in patients that could cause bronchiectasis.

Scientists note that “the bacterial flora appear to change with progression of disease.”

Early diagnosis and treatment can help stop the disease from progressing and causing severe complications. Treatment for symptoms can improve the patient’s quality of life.

Many of the treatment options developed have been learned from treating patients with cystic fibrosis.

Treatment aims to:

  • deal with underlying conditions or new infections
  • remove mucus from the lungs
  • prevent complications from developing

There are different forms of treatment.

Chest physical therapy (CPT)

Also known as “chest-clapping” or “percussion,” this is normally carried out by a respiratory therapist.

The patient will either sit down with their head downturned or lie face-down. Gravity helps the mucus to shift.

The therapist repeatedly pounds on the chest and back to loosen mucus and enable coughing. This can be done manually, with the hands, or using a device.

Examples of devices include:

  • an electric chest clapper, also known as a mechanical percussor
  • an inflatable therapy vest that uses high-frequency airwaves to shift mucus to the upper airway
  • a mask that causes vibrations to remove mucus from the walls of the airway

Studies indicate that such techniques may slightly improve the lungs’ ability to get rid of sputum, improve lung function, and enhance quality of life, compared with not using these techniques.

Adding in pulmonary rehabilitation may further improve the ability to exercise and quality of life.

Hydration

Consuming plenty of fluids can help keep mucus thinned out, less sticky and easier to cough up.

Medications

Antibiotics are used to treat infections. They may be given intravenously or by mouth, normally for 14 days. Another possibility is inhaled antibiotics, but these may have adverse effects, and more research is needed into their use.

Expectorants and mucus-thinners can help loosen mucus and support coughing.

Inhaled corticosteroids can treat inflammation of the airways that leads to wheezing or asthma.

A bronchodilator relaxes the muscles around the airways. The medicine is breathed in through an inhaler and nebulizer. Used before CPT, these may increase the benefit of the therapy.

Delivering the bronchodilator directly to the airways enables it to work quickly.

Oxygen therapy

Oxygen therapy, delivered through a mask or nasal prongs, can raise oxygen levels. This can be done at home or in a hospital. It is used in severe cases.

Surgery

Surgery may be suitable if:

  • only one part of the airway is affected, so it can be removed
  • there is bleeding in the airway that needs to be stopped

Severe cases may require a lung transplant to replace the diseased lungs with a healthy set of lungs.

This is more common if bronchiectasis results from cystic fibrosis.

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If an adult or a child gets a foreign object in the airway, they should seek medical help to avoid long-term complications.

It is important to seek early treatment for any respiratory condition that could lead to bronchiectasis.

Both adults and children should seek medical help at once if they accidentally inhale a foreign object.

Vaccinations can help prevent measles and whooping cough, childhood diseases that can progress to bronchiectasis.

Avoiding toxic fumes, gasses, and cigarette or other smoke can help preserve respiratory health.

Anyone with a chronic medical condition that increases the risk for bronchiectasis should monitor their lung function and be aware of the early symptoms.

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CHRISTUS Mother Frances Hospital – Sulphur Springs Business News

Sulphur Springs, Texas, August 8, 2022 CHRISTUS Mother Frances Hospital – Sulphur Springs has ONE mission: To Extend the Healing Ministry of Jesus Christ. 

Back to School

Are you going through the checklist of things to take care of before returning your students to school?  Perhaps they need their annual vaccines or sports physical?  We want to help!

Call us at 903.885.3181 to schedule an appointment with a Pediatrician or Family Medicine provider today! 

Pulmonary Rehabilitation

Do you need help managing your lung condition? Pulmonary rehabilitation can help. Pulmonary rehab is a program that can help you learn how to breathe easier and improve your quality of life. You can benefit from pulmonary rehab if you have:

  • Emphesema
  • Ashthma
  • Chronic bronchitis
  • Bronchiectasis
  • Cystic Fibrosis
  • A Neuromuscular disease (such as Multiple Sclerosis or Parkinson’s Disease)
  • Lung Cancer
  • History of smoking
  • Post lung surgery
  • Post COVID shortness of breath 

Pulmonary rehab cam make a difference. It is a safe, smart way to help you: decrease symptoms like being short of breath, coughing and wheezing. It can help you breathe better, get stronger, decrease stress, and reduce the risks of future lung problems and related hospital admissions. Pulmonary rehabilitation is designed to help increase strength, endurance, and overall health through exercise, education, diet, and support while decreasing patients’ shortness of breath. Ask your physician for a referral to CHRISTUS Mother Frances – Sulphur Springs’ Pulmonary Rehabilitation Program 903.439.4141

Sports Medicine

FREE Saturday Athletic Injury Clinic for student athletes of all ages is back this month! Starting August 20th, Saturday sports injury clinic will be held every Saturday from 9am to 11am, on August 20 through November 12. Student athletes in Hopkins County from 7th grade to college age will be able to get a free exam and x-ray to determine a plan of care to treat their injury. The clinic will be held at our CHRISTUS Trinity Clinic Orthopedics, Medical Building 5, at 103B Medical Circle in Sulphur Springs. For more information about our Sports Medicine program, or Orthopedic services, please call 903.885.6688.

COVID Vaccine Clinic Dates:

Net Health continues to offer Adult and Pediatric vaccines and boosters every three weeks at the clinic on 100 Medical Circle in Sulphur Springs. The clinic will be held on the following dates: August 22 – 26, September 19 – 23, and October 17 – 21. You may walk in from 10am to 3pm daily. No appointment is necessary.  

# # #

CHRISTUS Trinity Mother Frances Health System includes CHRISTUS Mother Frances Hospitals – Tyler, South Tyler, Jacksonville, Winnsboro and Sulphur Springs, the CHRISTUS Trinity Mother Frances Louis and Peaches Owen Heart Hospital – Tyler, CHRISTUS Trinity Mother Frances Rehabilitation Hospital a partner of Encompass Health, Tyler Continue CARE Hospital at CHRISTUS Mother Frances Hospital, a long-term acute care facility, and CHRISTUS Trinity Clinic. CHRISTUS Trinity Clinic is the area’s preferred multi-specialty medical group, with more than 400 Physicians and Advanced Practice Providers representing 36 specialties in 34 locations serving Northeast Texas across 41 counties. For more information on services available through CHRISTUS Trinity Mother Frances Health System, visit christustmf.org

Bed count – 402 – CHRISTUS Mother Frances Hospital – Tyler

Bed count – 8 – CHRISTUS Mother Frances Hospital – South Tyler

Bed count – 25 – CHRISTUS Mother Frances Hospital – Jacksonville

Bed Count – 96 – CHRISTUS Mother Frances Hospital – Sulphur Springs

Bed count – 25 – CHRISTUS Mother Frances Hospital – Winnsboro

Bed count – 94 – CHRISTUS Trinity Mother Frances Rehabilitation Hospital

Bed count – 96 – CHRISTUS Trinity Mother Frances Louis and Peaches Owen Heart – Tyler

Bed count – 51 – Tyler Continue CARE Hospital at CHRISTUS Mother Frances Hospital

 

Contributed by Jennifer Heitman

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This is a complete document on AirPhysio reviews and AirPhysio complaints. This document will give you all the details about this product before you buy it so that you can compare its pros and cons with other similar products on the market.

Say goodbye to a Viral cough that won't go away! Use this ASAP

Are you searching for something which will improve your breathing naturally? v

There are so many people in our world who suffer from unbearable coughs that come out of nowhere. These coughs not only block your standard breathing patterns but also make mucus accumulate in your body and make it uncomfortable. But, with the modern innovations in the medical industry, there are so many breathing and mucus-removing aids on the market.

In fact, if you go to a pharmacy and inquire about a product that lets you breathe more comfortably, they will present you with a dozen choices. Some of these products indeed work better. But there are also some devices that don't work correctly to give the benefits it promises so grandly.

These are the devices that con people into a money-wasting investment without any return for the buyer. Not only do they waste your money, but they will also prevent you from buying the best device that will get you out of your medical condition.

Therefore, it is crucial that you do your homework and research the products available on the market. With the help of the research, you can compare and contrast them until you find the best item that suits you.

AirPhysio, a new arrival on the market, is not that popular among the people. But after going through the few thousands of reviews posted by users, it becomes apparent that this is one of the list toppers in the medical industry.

This is our thoroughly researched document on AirPhysio UK we created to help you save time while doing the research on the best devices that could help you get rid of viral coughs and mucus accumulation. The followings are the main areas that we will touch on with this document.

  • What is AirPhysio device (AirPhysio COPD)
  • How does AirPhysio work? (does AirPhysio really work?)
  • How to use AirPhysio UK
  • AirPhysio side effects
  • AirPhysio UK reviews and AirPhysio complaints
  • AirPhysio where to buy
  • AirPhysio cost

Breathing is made more accessible by how AirPhysio works, which clears the lungs of accumulated mucus and increases lung capacity. AirPhysio is a very efficient tool to clear phlegm and expand the lungs. The OPEP positive expiratory pressure items are devices that can be used to remove and clear mucus from the lungs naturally.

In addition, AirPhysio is a highly regarded OPEP (oscillating positive expiratory pressure) device that increases lung volume to aid secretion mobilization, mucus clearance, and expansion.

Even "normal" tasks can be tiring when you have an ongoing respiratory condition that causes your airways to become blocked with thick fluids or mucus.

Have you ever tried to climb a short flight of stairs and got out of breath? Alternatively, if you bring your groceries from the car into the house?

How about when you sleep? Whether you slept 8, 10, or 12 hours last night, do you always feel exhausted?

According to medical professionals at WebMD, if you answered positively to any of these questions, you may have an above-average buildup of mucus in your lungs.

And you feel tired simply because your body is working twice as hard, if not ten times harder than usual.

Global news, New York City, NY Breathing problems have become more common due to poor lifestyle choices and naturally occurring conditions such as asthma, COPD, and bronchiectasis. Researchers have developed a therapy and treatment tool to help people with lung diseases such as cystic fibrosis, COPD, and asthma breathe easier and live better.

With a counted 1 billion people suffering from respiratory problems worldwide, They will only be able to feel better and breathe more easily organically thanks to this amazing invention.

What's This Incredible Airphysio?

To help you breathe better naturally, AirPhysio uses oscillating positive expiratory pressure or OPEP.

You exhale while keeping the AirPhysio mouthpiece close to your mouth. AirPhysio builds up positive pressure in your lungs as you exhale. Phlegm is loosened from the walls of your airway by the positive pressure, enabling you to cough it out spontaneously. You eventually breathe normally and experience better, clearer breathing.

Mucus in your airways may be the cause of your breathing difficulties. Your airways may become blocked with mucus, which will make it challenging to breathe. You can purge this mucus, according to AirPhysio, without taking a decongestant. Your airway receives all the advantages of a decongestant without the medication.

A unique product on the market works similarly and is very similar to an asthma device. It's similar to an asthma device but works more like an alcohol control device, so it could be considered a hybrid between the two.

By taking numerous deep breaths into the compact AirPhysio breathing therapy device, you can improve your breathing and the function of your lungs. According to the manufacturer, this removes mucus and other impurities and particles and should make your breathing and coughing work more effectively.

AirPhysio responds promptly. The majority of users claim that the device starts to function nearly. After breathing and breathing using this AirPhysio, you should be glad to notice much clearer breathing and lungs.

According to the official website, medical professionals advise AirPhysio for respiratory disorders. The website is replete with endorsements for using AirPhysio for illnesses such as;

  • Asthma
  • Bronchiectasis
  • Emphysema
  • chronic bronchitis
  • COPD
  • Atelectasis

and other respiratory diseases from respiratory experts, pulmonologists, and others.

The Australian-made and owned AirPhysio Australia has received awards, including the Optus MyBusiness Start-up Business of the Year Award and the 2017 Best Product Award at the YIWU Imported Commodities Fair in China.

The oscillating positive expiratory pressure (OPEP) device known as AirPhysio aids in lung expansion and mucus clearance. This AirPhysio can use as an additional treatment to help patients avoid lung problems after surgery (i.e., heart and abdominal surgery). Using the AirPhysio device supports secretory mobilization, avoids atelectasis, and increases postoperative lung volume in patients.

The AirPhysio is a proven, drug-free, electronics-free pulmonary therapy device approved by Griffith University. You can use this AirPhysio anytime and anywhere, so don't worry.

The only downward catch with this device is that you can not find it in any of the local pharmacies or malls in your neighbourhood. The only legitimate place the creator sells this product is through if own official website. The manufacturer attested that it is the only place you can find this product.

He has done this to prevent the following situations.

  1. To prevent customers from getting into scams that imitate the physical appearance of the AirPhysio device
  2. To control the highly riding demand that flows from everywhere in the world
  3. To give the users discounts and money back guarantee

Therefore, always remember that the only place you can find this product is from the manufacturer's website. So the next time you see AirPhysio amazon or AirPhysio ebay, keep in mind those products are possibly scams, and the manufacturer does not give the money back guarantee for those products.

=> Visit 'AirPhysio Device' Official Website To Avoid Scams!

How Does This AirPhysio Help You Breathe?

How Does AirPhysio Work?

Knowing the science behind the medical device helps you understand it better and use it properly to attain the highest most benefits out of it. Consequently, we explain how to use AirPhysio and does AirPhysio work through this document, so it is advisable that you read the document from the start till the end.

The drug was designed to be more effective in treating respiratory conditions such as bronchiectasis, cystic fibrosis, COPD, and asthma. These conditions make it hard and uncomfortable for the body to excrete contaminated mucus from the lungs. Research has shown that asthma reduces your lung capacity by 5 to 25 ml per year and can shorten your life.

Breathlessness without effort occurs when lung capacity is so small that it cannot support many physical activities. Hence the demand for lung cleansing and expansion.

How did the oscillating positive expiratory pressure work in Airphysio?

The medical device works to oscillate positive expiratory pressure, which is the same process used in coughing. The process involves expanding the diaphragm and contracting it by closing and releasing the vocal cords to create an explosive ejection of air from the lungs and expel foreign objects.

AirPhysio combines diaphragm expansion with a stainless steel ball-bearing to form a cone seal to achieve a similar result. AirPhysio accelerates coughing by about 15 to 35 times per second, which helps the walls of the airways expand and contract faster, release mucus, and expand the lungs more effectively. An adequately positioned lung gives you more space to clear mucus and other debris.

The AirPhysio is a mucus clearance oscillating positive expiratory device, OPEP for short. It means the AirPhysio can help you whatever your breathing problem, whether chronic, seasonal, or just a bad cold! That's because it does more than help clear your airways. With the AirPhysio, you can strengthen your lungs!

To heck how it can allow for more effortless and unrestricted breathing, read the below section on how to use AirPhysio as well.

How To Use Airphysio

It would help you very much if you first understood how a device is used correctly to get all the benefits offered by the product. Not only will it give you the highest value of the item, but it will also help you remove any of the mucus accumulation in your lungs and breathe more easily.

Step 1: Remove the cap from your AirPhysio

Step 2: Take a deep breath as much as possible and hold it for a few seconds.

Step 3: Blow in at evenly spaced intervals for three to five seconds, or until your lungs are empty.

As you do so, the AirPhysio's ball bearing vibrates up and down rapidly, creating thousands of tiny air vibrations and positive pressure that "shake loose" thick mucus in your airways and lungs. But soon after, your body can cough effectively and clear the accumulated phlegm.

What's Inside Airphysio?

The AirPhysio gadget is patented. It shows that it has a distinctive design that sets it apart from other breathing training systems. The device consists of a shield, a steel ball, and a cone-shaped object.

You take off the protective cover of AirPhysio and take a deep breath. The steel ball and circular cone's air resistance will help break up mucus in your lungs. The symptoms and diseases of respiratory conditions can be managed without medication or surgery.

This Small Device Will Give Your Soothing Breathing Back

Benefits You Get When Using Airphysio

  • Clear the airways of mucus

AirPhysio clears the airways of mucus. By clearing your lungs and airways of mucus, the device makes breathing easier. It will stop you from being over exhausted and short of breath as soon as you engage in the most negligible possible work and will help you get rid of prolonged cough.

  • Unblock Congested and Semi-Congested Airways

Breathing can be made difficult by obstructed and semi-congested airways. With the help of AirPhysio, your ability to breathe will be improved. AirPhysio can help you reach your maximum lung capacity by unclogging a congested airway. You may have phlegm in and around your airways if you've found it difficult to breathe. Using the AirPhysio device will naturally unclog your lungs so that you can cough and remove the accumulated mucus in your organs. This way, every breath you take in will go to the lungs, which are now working at their maximum level.

According to AirPhysio, most users breathe significantly better after just a few breaths. The oscillation technology will create a natural pressure which helps remove the phlegm in your body's organs. You will feel relief from the next moment when you start using the device.

  • The work continues overnight

AirPhysio has both immediate and long-term benefits. After the first, you will find that breathing is more accessible.

Your lungs will become visibly more apparent, stronger, and healthier with regular use of AirPhysio. The more you are using AirPhysio, the more benefits you will see.

Trusted, advocated for, and utilized by hundreds of pulmonologists to assist individuals who are having trouble clearing phlegm and deep breathing.

  • Absolutely No Drugs, Safe and Effective

Your lungs can now be cleared and expanded without toxins, chemicals, or steroids. Several numbers of research have been done to support the science, making it both highly effective and completely safe. 2

AirPhysio's on-the-go design makes it easy to carry wherever life takes you! Just take it out of your pocket, give it a quick tug, and put it back in. It's that simple-no need for batteries or refills.

Due to its smaller size and weightlessness, you can carry it in your bag or purse whenever you are going out. Therefore, no matter where you go or where you are, you will have the AirPhysio to help you breathe much more comfortably.

30-DAY SATISFACTION GUARANTEE & 1-YEAR WARRANTY - You can quickly return AirPhysio if, for any reason, you are not completely satisfied.

=> Get Your 'AirPhysio Device' Via Official Website To Avoid Scams!

Which Conditions Can AirPhysio Help You With?

Before buying the product, make sure you are one of the people suffering from the following illnesses. They are the most famous types of diseases that it relieved with the help of AirPhysio NHS (AirPhysio Canada ).

If you do not find your disease among the list items below, consult your doctor to make sure you can also be benefitted from using this device. AirPhysio is promoted as a therapeutic and preventative measure for the following ailments.

  • Flu
  • Typical cold
  • Asthma
  • Atelectasis
  • Bronchiectasis
  • CF - Cystic fibrosis

If you think this product can give you positive effects and relieve you from your suffering, place your orders right away on the manufacturer's official website. At the moment, several discounts are also running on the website.

Does AirPhysio Work?

Given this, devices like AirPhysio appear to be reliable and very efficient. However, keep in mind that AirPhysio may not be able to address the underlying cause of mucus buildup in your lungs. Get treatment if you have a lung condition.

Nevertheless, AirPhysio can significantly improve your quality of life during therapy. AirPhysio can still help you feel better, although it may not treat atelectasis or cystic fibrosis directly.

AirPhysio can also help you prevent illness and difficulties with your current condition by keeping your airways clear and improving oxygenation.

Overall, research on OPEP devices seems very promising, although more research is needed to get a clear picture.

How Can I Get AirPhysio At The Best Price?

AirPhysio Where To Buy?

The AirPhysio is so popular that over 60,000 have been sold to date in over 15 different countries!

The 30-day satisfaction guarantee is the best. In other words, you are taking absolutely no financial risk by trying it out for 30 days, and it will also be delivered right down to your doorstep!

Here's how to order an AirPhysio device right away:

To access the website page, click this link. Choose the AirPhysio plan that works best for you (remember the 30-day money-back guarantee!) When you start using AirPhysio, breathe more freely and comfortably by getting your AirPhysio!

Click the button below to check availability in your location now.

The AirPhysio official website offers the cheapest AirPhysio plans. You will find the best discounts there, especially if you want to buy several AirPhysios.

They're having a unique discount right now while this review is being written! You only pay for 3 AirPhysio devices when you buy 5 (40 per cent savings). And you would pay for two devices when you buy 3. (33 per cent savings). Shipping within the US is also free!

When you visit the manufacturer's website, do not hesitate to check out the AirPhysio video posted on the site. It is the simplest method to get to know more about this simple device while also checking out how other users feel after using AirPhysio only for a couple of days.

It is the cheapest AirPhysio which works better than any other treatment method used to clear the airways of mucus. The thousands of five-star AirPhysio UK reviews are proof of it.

=> (SPECIAL OFFER) Click Here To Order The 'AirPhysio Device' For The Best Discounted Price Today From The Official Website!

It's Shallow When You Come With AirPhysio Pricing, Which Will Save Your Life

AirPhysio Cost

AirPhysio costs about $59.99 per unit, although the price drops when 3 or 5 units are ordered.

** Please note - It's wise to keep in mind that the following AirPhysio prices, discounts, and bundle offers we have mentioned could be temporary, and the manufacturer has the sole right to change them at any time that he, please. These changes could take place without prior notice. Therefore place your orders before these discounts run out of time, and you miss them.

  • 1 unit: $59.99 + $5.99 shipping
  • 3 units: $119.98 + free US shipping
  • 5 units: $179.97 + free US shipping

Order directly from the official website to get the best possible prices for AirPhysios. Each unit is designed for use by one person. You can use this any number of times.

Only the official manufacturer website is where you may get Airphysio, not other retailer websites like AirPhysio Amazon!

Is AirPhysio Legit

The fair treatment for phlegm buildup and improved breathing is AirPhysio. Despite their limitations, research has shown that OPEP devices can help users breathe more accessible, clear phlegm from their lungs, and generally live better. The award-winning AirPhysio design has also been praised for its ability to relieve the symptoms of respiratory conditions, such as;

  • Asthma
  • Atelectasis
  • Bronchiectasis
  • Emphysema
  • COPD
  • chronic bronchitis, and others.

We also wanted to reiterate that you should always consult your doctor before making any health-related decisions. So if you're facing any trouble, discuss breathing issues with your doctor. AirPhysio will likely make your life easier, but it may not be able to address the root cause of breathing problems.

This product is featured on many social media platforms, TV channels, magazines, etc. The best way to explain the item in short form is;

  • The OPTUS awards winner in 2017
  • Trusted and recommended by pulmonologists
  • Patented product
  • One year warranty for every unit you purchase
  • Proudly made in Australia

What You Can Expect After Using Airphysio

irPhysio is a patented, award-winning device recommended by pulmonologists and healthcare professionals for better breathing. Some medical professionals recommend AirPhysio for specific breathing problems. Others advise it for anyone looking to expand their lung capacity or improve their ability to take a full breath.

The creators of AirPhysio claim that problems with clearing mucus can result in an annual loss of 11 ml (1 shot glass) of lung function. You lose a little lung capacity if the mucus remains in your lungs every year without being cleared. It can lead to serious respiratory problems if left untreated.

An increase in mucus could indicate a problem. Additionally, it may develop naturally due to dietary or lifestyle choices. Breathing might become challenging when mucus accumulates.

What Negative Impacts Does The AirPhysio Have? - AirPhysio Side Effects!

The use of the AirPhysio has no documented AirPhysio complaints. There are no harmful side effects because it doesn't contain any chemicals or drugs. Several customer testimonials supported this claim, and the product underwent rigorous testing in Australia before being distributed to the rest of the world.

AirPhysio Reviews - AirPhysio NHS

With the help of the AirPhysio device, you can clear your lungs of mucus and expand your lung capacity.

This Australian-made device breaks up mucus in the airways. It's designed for smokers who want to regularly clear their lungs and those with lung conditions that worsen mucus buildup.

There are no medications in the AirPhysio, making it suitable for everyone. There are almost no adverse effects as there are no dangerous chemicals or hidden substances. Furthermore, no undesirable side effects of AirPhysio are known or expected in the long term. It is portable and lightweight, making it easy to carry.

Get AirPhysio UK from the official website to avoid scams.

How Much Does AirPhysio Cost? - Cheapest AirPhysio In The UK

You have to decide whether to buy something once or in larger quantities. The advantage of buying in bulk is that it reduces the cost per unit. See the following discounted prices.

  • Pound 63.86 for 1 AirPhysio gadget plus applicable shipping and handling charges.
  • 3 AirPhysio devices for Pound 42.57 each plus free shipping

Order AirPhysio UK from our official website!!!

How Much Does AirPhysio Cost? - Cheapest AirPhysio In Australia

Price From AirPhysio Australia

You have to decide whether to buy something once or in larger quantities. The advantage of buying in bulk is that it reduces the cost per unit. See the following discounted prices.

  • $69.99 for 1 AirPhysio device plus applicable shipping and handling charges
  • 3 AirPhysio devices for $46.66 each plus free shipping

Click here to go to their official website to purchase an AirPhysio Device with unbelievable discounts.

AirPhysio Reviews Consumer Reports

treatments or had violent fits of coughing for three weeks, he still had trouble clearing any phlegm. Eventually, he discovered AirPhysio and could finally cough it up with just a few uses. He earned his lungs throughout the day and hasn't coughed since. He claimed he now intends to buy respirators like this for everyone he knows who has lung and breathing problems and share that information with their doctor.

Another AirPhysio user adds that she has severe asthma, and her airways are permanently blocked. Since only steroids seemed to help, she found AirPhysio and has taken it ever since. Her airway is now unobstructed, and she can breathe quickly and pleasantly. Since taking steroids is unhealthy in the long term and pharmacological preparations should be avoided if possible, AirPhysio can only advise everyone with severe asthma.

Another user of the AirPhysio respiratory therapy gadget claims to be a registered nurse and is very happy with it. After brain surgery, her daughter-in-law developed pneumonia and pleurisy. She could only be cured, and her lungs are now entirely free, thanks to AirPhysio. She advises everyone, including athletes, to use this respiratory therapy tool.

=> Click Here To Get Your 'AirPhysio Device' From The Official Website! - Backed By 87,610+ Five Star Reviews!

Final Thoughts - AirPhysio UK Reviews

GetAirPhysio is a distributor of the AirPhysio OPEP respiratory training device. By removing mucus from your airways and strengthening your lungs, AirPhysio helps improve your breathing at natural levels.

Numerous pulmonologists and other professionals promote AirPhysio as a treatment for breathing problems. The device is advertised as an aid in treating and preventing respiratory diseases.

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We report a female infant who was born at 41+6 weeks of gestation to a consanguineous parent, and the initial newborn examination was within normal. At 12 hours of age, she developed tachypnea; with desaturation, she had continuous thick whitish oral secretion. Admitted to the neonatal intensive care unit (NICU) for further management, her initial blood investigation, including blood gas and chest X-ray, was normal. Due to the persistent unexplained respiratory distress with a normal chest X-ray, we obtained a further history from parents with three siblings with respiratory symptoms but no definitive diagnosis. The genetic testing of whole-exome sequences (WES) confirmed a homozygous variant c.804_806del, p.(Lys268del) in the RSPH9 gene that causes primary ciliary dyskinesia (PCD). Her three siblings were tested and found to have the same genetic mutation.

Introduction

Primary ciliary dyskinesia (PCD) is a rare autosomal recessive genetic disorder that causes defects in the function and/or structure of the cilia lining the respiratory tract, fallopian tube, and flagellum of sperm cells [1]. PCD is often underdiagnosed, and it is estimated to occur in 1/15,000-20,000 individuals [2-3]. Moreover, due to the high consanguinity rates, PCD is more common in Arab societies, although little is known about its actual prevalence and characteristics [4]. Patients with PCD may present with neonatal respiratory distress and/or laterality defects in about half of the cases. Studies have shown that more than 80% of neonate patients present with respiratory distress symptoms within the first 1-2 days of life, with most cases appearing 12 hours after birth [3]. In this article, we report an unusual case of respiratory distress in a full-term female infant. The diagnosis of primary ciliary dyskinesia was confirmed by genetic testing, which led to the same diagnosis in three siblings at different ages. 

Case Presentation

A female infant was born at 41+6 weeks of gestation via an emergency Cesarean section due to abnormal fetal heart rhythm. The infant's mother was diabetic. The parent is a first-degree cousin. She had three siblings diagnosed with bronchial asthma and chronic otitis media. Antenatal ultrasounds were unremarkable, and the maternal laboratory findings are as follows: hepatitis B was negative; group B Streptococcus was positive. Her appearance, pulse, grimace, activity, and respiration (APGAR) scores were nine and nine at one and five minutes, respectively, and her weight was 4 kg. Her vital signs were stable (temperature of 36.9ºC; heart rate of 150 beats/min; respiratory rate of 55 breaths/min; blood pressure of 66/40 mmHg; oxygen saturation of 96%), and the initial newborn examination presented normal results. At 12 hours of age, the baby started to be tachypneic; with desaturation in room air, she had continuous thick whitish oral secretions. A full sepsis workup was done. Complete blood cell count revealed a white blood cell count of 6,000/mL with a normal differential, hemoglobin of 15.8 g/dL, and platelet count of 250×103/μL. Her initial blood gas and chest X-ray were normal (Figure 1). 

An echocardiogram showed normal structure and function of the heart with no evidence of pulmonary hypertension. Initially, she was on a high-flow nasal cannula (HFNC) of eight liters per minute with a fraction of inspired oxygen (FiO2) of 35%. She was treated for clinical sepsis with five days of antibiotics. Her respiratory distress improved with respiratory support. She needed oxygen for a total period of 14 days, and then she was observed for two days without supplemental oxygen before being discharged. The genetic testing was requested based on unexplained respiratory distress with normal chest X-ray and normal echocardiography. The whole-exome sequences (WES) confirmed a homozygous variant c.804 to 806del, p.(Lys268del) in the RSPH9 gene (OMIM: 612648) that causes PCD. Her three siblings were tested for the same gene and confirmed the same genetic mutation.

Four months later, the patient was admitted to another hospital with fever and respiratory symptoms for two days. After a month, she presented to the emergency department with fever and increased work of breathing; pneumonia was confirmed and treated with HFNC 14 L/min with FiO2 of 25%. Intravenous antibiotics were continued for ten days, bronchodilators and a 3% normal saline nebulizer with chest physiotherapy were provided. Chest X-ray showed that the right upper lobe had collapsed (Figure 2). The respiratory culture isolated Streptococcus pneumonia, and the respiratory multiplex was positive for rhino/enterovirus. After completing the antibiotic course, the baby was discharged home. Since then, the baby has done well; she only had to continue chest physiotherapy and hypertonic nebulizer 3%. All her siblings have started to follow up with the pulmonologist after confirming their diagnosis.

Discussion

Although infants with PCD are often diagnosed with transient tachypnea of the newborn (TTN), the clinical presentation in PCD is different with later onset of respiratory distress, longer duration of oxygen therapy use, and higher frequency of atelectasis and/or lobar collapse upon chest imaging [1].

There is no single gold standard diagnostic test for PCD; the current diagnosis requires a combination of investigations that may not be feasible in all hospitals. Those tests include nasal nitric oxide, high-speed video microscopy analysis, transmission electron microscopy, high-resolution immunofluorescence analysis, and genetic testing [5].

The current therapies for PCD are extrapolated from cystic fibrosis (CF) and patients with non-CF bronchiectasis and lack validation for PCD-specific use [1-6]. The main goal of the treatment is to manage the condition symptomatically, clear the trapped mucus from the airways, and treat the respiratory infection using antibiotics. PCD patients need regular follow-up visits with pediatric pulmonology, otolaryngology, and respiratory therapists. The progression of lung disease varies and is affected by the time of diagnosis, the ability of medical treatment to control symptoms, and the prevention of complications that affect the quality of life [7].

In this case, we reported a full-term neonate with unexplained respiratory distress who needed oxygen therapy for 14 days. Later, her genetic testing was positive for a mutation in the RSPH9 gene, causing PCD. Our patient did not have a laterality defect on chest X-ray and abdominal ultrasound, which made the diagnosis challenging. However, careful history taking of the older siblings, who also had unexplained neonatal respiratory distress and her needing oxygen for a period after birth as well as having chronic wet cough, increased our suspicion about the diagnosis. 

Casey et al. reported similar cases of a family with three individuals who had respiratory distress symptoms as well as PCD, confirmed with genetic testing, associated with laterality defects, which is considered to be due to a homozygous missense variant in CCDC103 on chromosome 17 according to exome sequencing [8]. Another study presented a group of term neonates who had PCD and a history of neonatal respiratory distress [9]. The study showed that cases with PCD required more oxygen therapy for a longer duration and had a later onset of neonatal respiratory distress and a higher frequency of lobar collapse and situs inversus.

It was suggested that when encountering term neonates with unexplained respiratory distress, PCD should be considered in those with lobar collapse, situs inversus, and/or prolonged oxygen therapy (>2 days); moreover, treatment should be initiated immediately to reduce the risk of complications [9]

Conclusions

Primary ciliary dyskinesia (PCD) is a rare autosomal recessive disorder that can present with respiratory distress at birth or in the first few days after birth. Unexplained respiratory distress with the presence of a family history of undiagnosed respiratory symptoms should prompt further investigation for a genetic disease. Whole-exome sequences are the modality of choice for the diagnosis of PCD. The main goal of the treatment is to manage the condition symptomatically, control infections, and clear the trapped mucus from the airways, which can slow the progression of the disease. Careful history taking is vital; in this case, the diagnosis of PCD in three siblings at different ages shows us how PCD is still underdiagnosed and can be easily missed for many years.



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Lungs, the main organ in the respiratory system, expand and contract about a thousand times a day providing an efficient gas exchange [1]. Diseases or pathologies in the lungs and airways that develop slowly and worsen over time are called chronic respiratory diseases [1]. Chronic obstructive pulmonary disease (COPD), asthma, and occupational lung diseases are among the most common and major chronic respiratory diseases [2]. According to the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017, chronic respiratory diseases are one of the leading causes of death and disability in the world, with the highest prevalence in high-income regions [3]. Nearly 545 million individuals (7.4% of the world’s population) live with chronic respiratory problems [3]. The economic burden associated with asthma, COPD, and other chronic respiratory disorders is among the highest compared to other chronic diseases [4].

According to the Global Initiative for Asthma, 2019, asthma is characterized as chronic airway inflammation and hyperresponsiveness with variable expiratory airflow limitation [3]. It is the most common non-communicable disease in children, and 40% of children and 50% of adults diagnosed with asthma have uncontrolled disease, representing an unmet medical need [3,4]. Despite differences in etiology, symptoms, and prognosis, asthma and COPD share the common pathogenesis of airway inflammation [5]. Medications that selectively target the disease pathology will increase the chances of therapeutic success [5].

Phosphodiesterase (PDE) is an enzyme involved in the pathogenesis of various chronic inflammatory diseases and degenerative diseases in humans [6]. PDE acts by hydrolyzing the intracellular nucleotide cyclic adenosine monophosphate (cAMP) and cyclic guanosine-5-monophosphate (cGMP) to its inactive compounds, adenosine-5-monophosphate (5-AMP) and guanosine-5-monophosphate (5-GMP), respectively [6]. PDE inhibitors are a major class of drugs currently being investigated as a treatment strategy for COPD, asthma, depression, cognitive and affective disorders, atopic dermatitis, and fragile X syndrome [7].

The selective phosphodiesterase 4 (PDE4) enzyme, which is encoded by four genes, is a member of the PDE superfamily of 11 subtypes [8]. As it is specifically found in inflammatory cells and airway smooth muscle cells, PDE4 inhibitors are considered a therapeutic target for inflammatory respiratory diseases such as COPD and asthma [8,9]. However, roflumilast is the only PDE4 inhibitor currently approved for the treatment of respiratory disorders and is used as a second-line medication for severe COPD with chronic bronchitis [6]. Other PDE4 inhibitors that have been approved include apremilast for psoriatic arthritis and plaque psoriasis and crisaborole for the topical treatment of atopic dermatitis [6].

Clinical data provide promising results for the potential use of PDE4 inhibitors in asthmatic patients [4]. Its effectiveness has also been tested for various other inflammatory respiratory diseases, including allergic rhinitis, non-cystic fibrosis bronchiectasis, and chronic cough [6,10]. However, PDE4 inhibitors are not approved as a treatment strategy for any other respiratory diseases except COPD [7]. This systematic review summarizes the recent evidence on PDE4 inhibitors concerning their therapeutic potential, limitations for approval as treatment options for respiratory disorders other than COPD, and the recent advances to overcome the limitations.

Methodology

The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines 2020 were followed in this systematic review, and the population, intervention, and outcome with or without a control (PICO) format was included in this study pattern [11].

Inclusion and Exclusion Criteria

All studies related to the topic, published in the English language, across the globe within the last five years (2017-2022) where the free full-text article is available or can be received from the author were included. The study population considered was humans without limitation of age or sex who were affected by respiratory disorders other than COPD. The overall effect of the selective PDE4 inhibitor therapy (intervention) on the disease outcome compared to the conventional treatment or placebo (control) or without any comparison group was assessed. All types of study designs were included without any restrictions. All other articles published before 2017, non-English-language studies, animal studies, non-full-text articles, book articles, and gray literature were excluded from the study.

Information Sources and Search Strategy

A detailed search was done on four databases, namely, PubMed, PubMed Central, Google Scholar, and ScienceDirect, using the relevant keywords. Medical Subject Heading (MeSH) search blocks with Boolean operators were used in the PubMed database search, and appropriate filters were used according to the availability in the selected databases. The data were searched from all databases lastly on April 16, 2022. The search strategy including the relevant keywords and MeSH terms used is listed in Table 1.

Database Search strategy Filters Search result
PubMed Asthma OR Bronchiectasis OR chronic cough OR (((“Asthma/drug effects” [Majr] OR “Asthma/drug therapy” [Majr] OR “Asthma/prevention and control” [Majr] OR “Asthma/therapy” [Majr] )) OR (“Bronchiectasis/drug therapy” [Majr] OR “Bronchiectasis/prevention and control” [Majr] OR “Bronchiectasis/therapy” [Majr] )) AND Phosphodiesterase 4 inhibitors OR PDE inhibitors OR Roflumilast OR (“Phosphodiesterase 4 Inhibitors/administration and dosage” [Mesh] OR “Phosphodiesterase 4 Inhibitors/adverse effects” [Mesh] OR “Phosphodiesterase 4 Inhibitors/therapeutic use” [Mesh] OR “Phosphodiesterase 4 Inhibitors/toxicity” [Mesh]) Humans, English language, 2017–2022, free full text 268
PMC Asthma OR Bronchiectasis OR Chronic cough AND PDE 4 inhibitors Five years 355
Google Scholar Asthma OR Bronchiectasis OR Chronic cough AND PDE 4 inhibitors 2017–2022, review articles 2,290 (First 500 records were identified)
ScienceDirect PDE4 inhibitor therapy in Non-COPD respiratory diseases 2017–2022, review and research articles 107

Data Collection and Study Selection

Study selection was done by two researchers independently according to the inclusion and exclusion criteria. Full articles were analyzed extensively, and any discrepancies were reevaluated and reassessed by both researchers to reach common ground. Studies that were focused on our topic, fit our inclusion and exclusion criteria, and were of good quality were chosen for this study.

Results

Among the identified 1,230 studies, 177 duplicates were removed using the EndNote X9 version and manually. The remaining 1,053 articles were initially screened based on the title and abstract. Among them, 994 studies were excluded as they were irrelevant to the study, and the remaining 59 studies were sought for retrieval for further screening. Only 35 studies remained for the assessment because 24 studies were not retrieved. Full articles of 35 studies were assessed extensively based on the eligibility criteria and quality. Finally, a total of 11 studies were included in this systematic review. Figure 1 depicts the search process used for this review in the form of a PRISMA flow diagram [11].

Quality Appraisal

The risk of bias in individual studies was reduced by assessing the quality by two independent researchers with the use of relevant quality assessment tools. Studies that had a quality above 70% or get an overall “Low Risk” in risk of bias were included while the studies that did not fit the criteria or that we found biased were excluded. The summary of the quality appraisal process of selected studies is included in Table 2.

Quality assessment tool Type of study Total score Accepted score (>70%) Accepted studies
Assessment of Multiple Systematic Reviews (AMSTAR 2) [12] Systematic review and Meta-analysis 16 12 Luo et al. (2018) [9]
Scale for the quality Assessment of Narrative Review Articles (SANRA 2) [13] Narrative review 12 9 Chinn et al. (2020) [4] Facchinetti et al. (2021) [5] Kawamatawong et al. (2021) [6] Phillips et al. (2020) [8] Syfridiana et al. (2021) [14] Zuo et al. (2019) [15] Li et al. (2018) [16] Matera et al. (2021) [17]
Cochrane risk-of-bias tool (RoB 2) [18] RCTs 7 5 (Low Risk) Bjermer et al. (2019) [19] Juthong et al. (2022) [20]

Data Analysis

This systematic review describes the study results based on their outcomes, applicability, and limitations as a narrative synthesis because inter-variability was noted between the studies such as heterogeneity of study designs, participants, interventions, and outcome measures. All articles included in the study were reviewed and analyzed extensively and tabulated into (1) randomized controlled trials (RCT), (2) systematic review and meta-analyses, and (3) review articles. Table 3 summarizes the relevant results extracted from the selected studies.

Study source Study name Study type Study objective Related conclusion
Chinn et al. (2020) [4] Cyclic AMP in dendritic cells: A novel potential target for disease‐modifying agents in asthma and other allergic disorders Literature review Review the role of dendritic cells and cAMP as potential disease-modifying therapies in asthma and other allergic disorders Propose to design drugs that selectively raise cAMP in dendritic cells as a novel disease-modifying therapy for allergic asthma
Facchinetti et al. (2021) [5] Tanimilast, a novel inhaled PDE4 inhibitor for the treatment of asthma and chronic obstructive pulmonary disease Literature review Review main preclinical and clinical studies conducted during the development of Tanimilast and identify subgroups of patients with possible therapeutic success Tanimilast demonstrates good anti-inflammatory properties in both COPD and asthma. Phase IIa clinical studies used in asthma demonstrated significant LAR to inhaled allergens and numerical reduction in sputum eosinophilia
Kawamatawong et al. (2021) [6] Phosphodiesterase-4 inhibitors for non-COPD respiratory diseases Literature review Review the evidence on the effectiveness of Roflumilast and other PDE4 inhibitors in chronic inflammatory respiratory diseases beyond COPD including certain COPD phenotypes with comorbidities Roflumilast and selective PDE4 inhibitors have demonstrated a broad spectrum of anti-inflammatory effects on chronic respiratory diseases including asthma, asthma-COPD overlap syndrome, and COPD with comorbidities. Further well-designed clinical studies will be helpful
Phillips et al. (2020) [8] Inhaled phosphodiesterase 4 (PDE4) inhibitors for inflammatory respiratory diseases Literature review Summarize the clinical structure, pharmacological, and clinical details of inhaled PDE4 inhibitors CHF 6001 as the only inhaled PDE4 inhibitor currently advancing through clinical development has promising results with minimal systemic adverse effects in phase II clinical trials in asthma
Luo et al. (2018) [9] Efficacy and safety of phosphodiesterase 4 inhibitors in patients with asthma: a systematic review and meta-analysis Systematic review and meta-analysis Evaluation of the effects of PDE4 inhibitors on clinical outcomes in patients with asthma Oral PDE4 inhibitors improve lung function, asthma control, and asthma exacerbations with the expense of increased adverse events. Oral PDE4 inhibitors including roflumilast 500 µg may be an alternative treatment to regular bronchodilators and inhaled controllers in patients with mild asthma
Syfridiana et al. (2021) [14] Roflumilast: review of phosphodiesterase-4 inhibitor as asthma therapy Literature review Determine the efficacy and safety of using roflumilast as a therapeutic option in asthmatic patients Numerous clinical studies conducted on the effectiveness of roflumilast therapy in asthma (phase I-III) demonstrated significant improvement in FEV1. Statistically, a significant difference was not noted between the doses of 250 and 500 µg of roflumilast. Combination therapy with montelukast demonstrated comparative improvement in lung functions and respiratory symptoms
Zuo et al. (2019) [15] Phosphodiesterases as therapeutic targets for respiratory diseases Literature review Discuss PDE subtypes and the role of selective PDE inhibitors in the therapeutic application for COPD and asthma PDEs are an attractive pharmaceutical target for COPD and asthma treatment. Dual PDE4/3 inhibitor (RPL554) demonstrated anti-inflammatory and airway-modulatory effects in phase I clinical trials. Further clinical studies to explore the real pharmaceutical target of RPL554 were recommended
Li et al. (2018) [16] Phosphodiesterase-4 inhibitors for the treatment of inflammatory diseases Literature review Summarize the chemical skeleton and pharmacological and clinical details of the licensed PDE4 inhibitors in the process Various adverse effects associated with PDE4 inhibitors are the primary bottleneck in new drug development. Three possible strategies to avoid this problem were described
Matera et al. (2021) [17] New avenues for phosphodiesterase inhibitors in asthma Literature review Discuss the progress made in recent years regarding PDE4 inhibitors in the treatment of asthma No PDE inhibitor has yet reached the market as a therapeutic option for asthma. The current focus is on the development of PDE inhibitors that interact simultaneously with different PDE types. CHF6001 and RPL554 are the PDE4 inhibitors under development for asthma to date
Bjermer et al. (2019) [19] Efficacy and safety of a first-in-class inhaled PDE3/4 inhibitor (Ensifentrine) vs Salbutamol in asthma RCT Investigate the dose-response and the pharmacology of a single dose of ensifentrine nebulizer suspension Single-dose ensifentrine demonstrated dose-dependent bronchodilation which is effective as a therapeutic dose of nebulized salbutamol and did not show the systemic safety issues of β2 agonists
Juthong et al. (2022) [20] Efficacy of roflumilast in bronchiectasis patients with frequent exacerbations RCT Assess the efficacy of roflumilast on the exacerbation of bronchiectasis Roflumilast did not significantly affect the rate of exacerbation or the quality of life. Improvement in FEV1 was noted in the roflumilast group compared to the placebo group

Discussion

This section describes the PDE enzyme, therapeutic benefits of PDE inhibitors, recent advances in the development of selective PDE4 inhibitors, and current evidence and future targets of their use in various respiratory diseases beyond COPD.

Phosphodiesterase and cAMP

PDE enzyme in mammals is classified into 11 subfamilies based on kinetics, substrate selectivity, and their distribution in cells and tissues [21]. It modulates intracellular signal transduction by catalyzing the hydrolysis of cAMP and cGMP into their inactive metabolites 5-AMP and 5-GMP, respectively [5,6]. Identification of this enzyme about 60 years ago opened the gates to an important area of clinical research as inhibition of this enzyme provides an enormous potential for therapeutic benefit in many pathological conditions [22]. Current evidence supports that different PDE subtypes have their own characteristics such as PDE1, PDE2, PDE3, PDE10, and PDE11 degrade both cAMP and cGMP; PDE5, PDE6, and PDE9 only degrade cGMP; and PDE4, PDE7, and PDE8 degrade only cAMP [22]. PDE4 and PDE5 are the most important isoforms related to respiratory disease [21].

cAMP is an intracellular second messenger that is produced by the conversion of adenosine triphosphate (ATP) by the enzyme adenylyl cyclase (AC) after activation of G-protein coupled receptors (GPCR) [21,22]. cAMP plays a key role in cellular function and its signaling which is compartmentalized within cells explains the vast area of action sometimes even opposing effects [21]. PDE inhibitors that prevent hydrolysis of this unstable compound provide therapeutic benefits by increasing cellular cAMP levels [21].

PDE4 Inhibitors and Roflumilast

Genetic encoding and tissue distribution classify the PDE4 enzyme into four subtypes, namely, PDE4A, PDE4B, PDE4C, and PDE4D [6]. The genes encoding these subtypes also encode several different isoforms (three-eleven) within the subfamily [15,22]. Even though PDE4 are mostly abundant in inflammatory cells, airway cells, and lung tissues, they are also present throughout the body, including, but not limited to, the brain, heart, kidney, skeletal muscle, skin, testis, and liver [6,15]. Evidence support that PDE4 isoform expression in lung tissue varies depending on their clinical status such as in patients with COPD and asthma compared to healthy individuals [15]. Regulation of fundamental functions is the key role of selective PDE4 inhibitors, which comprises stabilization of endothelial and epithelial barriers, modulation of the inflammatory response, and cognitive and/or mood function [22].

Roflumilast is the most extensively studied second-generation PDE4 inhibitor for respiratory diseases and is the only approved PDE4 inhibitor for respiratory pathology, i.e., COPD [6,8]. Compared to the non-selective PDE inhibitor theophylline, both roflumilast and its metabolite roflumilast-N-oxide are potent selective PDE4 inhibitors that act on inflammatory cells and the structural cells of the respiratory system involved in the pathogenesis of chronic respiratory diseases [6]. The pathophysiological basis of preventing inflammation by roflumilast has been studied extensively. Roflumilast acts on the lung macrophages inhibiting inflammatory cytokine release, eosinophils inhibiting reactive oxygen species formation (ROS), and neutrophils suppressing the release of their inflammatory mediators [6]. They also act on the airway smooth muscle cells and produce an inhibitory effect on contractile activity promoting bronchodilation [6]. A synergistic effect of dexamethasone on airway smooth muscle cells, when given in combination with formoterol, a long-acting β2 agonist (LABA), was also noted [6,23]. Some other effects of roflumilast on respiratory pathologies include (1) inhibition of profibrotic growth factor (TGF-β), (2) attenuation of fibroblast chemotaxis that promotes airway and lung fibrosis, (3) activation of cystic fibrosis transmembrane conductance regulator (CFTR) in airway epithelial cells, (4) inhibition of release of tumor necrosis factor-α (TNFα) by bronchial epithelial cells, and (5) decrease in the expression of MUC5AC (predominant mucin gene expressed in healthy airways and overexpressed in asthmatic and COPD patients) in human airway epithelial cells [6]. It also exerts favorable effects on the cigarette smoke-injured human bronchial epithelium by improving ciliary motility and increasing airway surface liquid (ASL) hydration, facilitating mucus dehydration and mucus clearance in COPD with chronic bronchitis and other suppurative airway diseases [6]. Figure 2 describes the mechanism of action of PDE4 inhibitors.

Despite its high potential to provide therapeutic benefit in many disease pathologies, only three PDE4 inhibitor drugs (roflumilast, crisaborole, apremilast) are currently being approved [8]. The main reasons identified for this delay in therapeutic success are the narrow therapeutic index and the intolerable adverse effect profile [8]. The most commonly observed adverse effects are nausea, diarrhea, abdominal pain, loss of appetite, weight loss, headache, and sleep disturbances [10]. Also, studies on the efficacy of roflumilast revealed that the maximum tolerated dose is near the bottom of the efficacy dose-response curve [8]. These have prompted current research to consider developing novel PDE4 inhibitors which enhance treatment efficacy and avoid adverse effects [7].

PDE4 Inhibitors in Asthma

Inhaled corticosteroids (ICS) and LABA are the mainstay of maintenance therapy in asthma. Despite their therapeutic efficacy, a considerable proportion of asthmatic patients still experience recurrent symptoms [24]. The epidemiological data on uncontrolled asthma and the economic burden per each asthma patient per year, which has been calculated as USD 1,000, highlight the necessity of novel therapeutic options in asthma management [22]. Even though researchers and clinicians repeatedly expressed the possibility of using PDE inhibitors in asthma therapy due to their effective bronchodilator and anti-inflammatory properties, none of the PDE4 inhibitors has entered the market as asthma therapy in the past three decades [17].

Studies on roflumilast demonstrated a reduction in late asthmatic response (LAR) and prevention of subsequent increase in bronchial reactivity following an allergen challenge. But a considerable effect on the acute-phase response (bronchoconstriction) was not demonstrated [25,26]. Further studies demonstrated improvement in lung functions of asthmatic patients when combined with ICS or montelukast [27,28]. Because ICS has a flat dose-response in airway caliber to high doses, adding on drugs such as LABA or montelukast is preferred over increasing the ICS dose and add-on LABA is shown to be more effective than add-on montelukast [6]. A short-term study done by adding roflumilast 500 µg and montelukast 10 mg to ICS/LABA compared to adding only montelukast 10 mg to ICS/LABA in patients with poorly controlled asthma showed comparative improvement in forced expiratory volume in the first second (FEV1) in the roflumilast group [14,27]. This potential benefit of improving lung function on FEV1 and forced vital capacity (FVC) by adding roflumilast can be explained as attenuation of airway inflammation for ICS and/or synergistic bronchodilator effect with LABA [6]. The mechanism of PDE4 inhibitors and LABA improving the clinical efficacy of glucocorticoids in inflammatory lung diseases has been explained as an interplay between the glucocorticoid receptor and the cAMP receptor pathway [29]. However, a paucity of further clinical studies on roflumilast in asthma therapy was noted due to its comparable efficacy to ICS with the expense of numerous adverse effects [6]. Further studies done in this field have identified three main strategies as effective to overcome these barriers. They are designing potent isoform-specific inhibitors or allosteric modulators, changing the route of administration by designing inhalational preparations and combining therapy with other medications [16]. Table 4 summarizes the details of other important PDE4 inhibitors studied in asthma.

Author and year Patient characteristics Intervention Duration Out come Comment
Singh et al. (2010) [30] Atopic asthma-ICS naive Inhaled isoform-specific PDE4B (GSK 256066) 87.5 µg versus placebo Seven days Demonstrated significant protective effects on both EAR and LAR to allergen challenge. No longer in the development process due to its poor pharmacokinetic properties.
Singh et al. (2016) [31] Atopic asthma-ICS naive Inhaled CHF6001 400 µg/1,200 µg vs placebo OD via DPI Nine days Demonstrated significant attenuation of LAR to allergen challenge- Non-significant reduction in sputum eosinophil count was noted Promising results warrant further research
Leaker et al. (2014) [32] Atopic asthma-ICS naive Oral MEM1414 600 mg BID vs placebo Two weeks Demonstrated significant reduction of LAR to allergen challenge. No effect was noted on EAR Associated side effects abandoned further research
Bjermer et al. (2019) [19] Asthma Nebulized ensifentrine 0.4, 1.5, 6, and 24mg vs salbutamol 2.5 and 7.5 µg vs placebo   Demonstrated significant dose-dependent bronchodilation compared to placebo. Efficacy was comparable to the therapeutic dose of nebulized salbutamol with good tolerability. Did not show β2 agonist-associated systemic adverse effects Promising results warrant further research

GSK256066, an inhalational isoform-specific PDE4B inhibitor, has demonstrated protective effects on both early asthmatic response (EAR) and LAR to inhaled allergens [8,30]. However, further studies on this drug were prevented due to its poor chemical properties which makes it difficult to exert a good pharmacological effect [8,30]. Tanimilast (CHF6001), an inhaled selective PDE4 inhibitor that is about seven times more potent compared to roflumilast, has demonstrated significant inhibition of allergen-induced LAR in atopic asthmatics with minimal adverse effects in phase II clinical trials [5,31]. This has reached phase III clinical development in COPD patients with good tolerability, safety profile, and no evidence of class-related adverse effects [5]. Another study on Tanimilast describes that it has a greater effect on Th1 cytokines compared to corticosteroids. This suggests its potential role in the management of severe asthma [33].

Dual PDE inhibitors were developed to achieve optimal anti-inflammatory and bronchodilator action at a concentration that does not cause unwanted adverse effects [17]. Ensifentrine (RPL554) dual PDE 3/4 inhibitor has effective bronchodilator properties compared to a therapeutic dose of nebulized salbutamol and good tolerability without any β2 agonist systemic safety issues associated with salbutamol [15,19]. Promising results shown in this first RCT deemed the necessity of further research to confirm the effect of this new medication.

Novel Therapeutic Targets of PDE4 Inhibitors in Asthma

Selectively raising cAMP in the dendritic cells is a proposed novel therapeutic approach for allergic asthma. This follows the concept of focusing treatment on a specific endotype of disease (a distinct molecular mechanism) rather than the phenotype (disease characteristics independent of the mechanism) [4]. Asthma endotypes can be classified according to the predominantly involved cellular inflammatory mediators (eosinophils, neutrophils, mixed granulocytic) or type 2 helper T cell (Th2) high (allergic asthma) or non-type 2 (Th2 low) asthma [4]. Dendritic cells, which play an important role in inducing Th2 differentiation, play a key role in allergic asthma. Therefore, selectively inhibiting the PDE4 enzyme in dendritic cells will provide endotype-specific therapy for allergic asthma [4].

The importance of exploring the PDEs that were not fully investigated in the past for their ability to induce bronchodilation is another new suggestion in the research world [17,34]. Evidence supports the ability of PDE8 and PDE9 to induce bronchial smooth muscle relaxation in animals [34]. Potentially druggable targets in inhibiting these PDEs, which simultaneously interact with other PDEs, create new opportunities for future researchers and will be a more fruitful approach for improving the care of asthmatic patients [17,34].

Multiple therapy fixed-dose combination inhalers that contain dual PDE inhibitors and hybrid molecules with other bronchodilators are considered an effective therapeutic option for asthma as they can provide three to four complimentary effects together [17]. Scientists have also considered the development of hybrid molecules specifically designed to have multi-functional ligands containing two or more pharmacophores [17]. Future research focusing on these advanced methods will bring new hope for physicians caring for asthmatic patients.

PDE4 Inhibitors in Allergic Rhinitis

Allergic rhinitis (AR) is an inflammatory disorder of the nasal epithelium which occurs due to allergen exposure. About 15-38% of patients with allergic rhinitis are diagnosed with asthma, and 6-85% of patients with asthma get nasal symptoms [10]. Even though the combination of oral/intranasal antihistamines and intranasal glucocorticoids is considered the mainstay of therapy, the recently described non-Th2-mediated inflammatory pathway of AR does not respond well to the current treatment [35]. The efficacy of roflumilast in the treatment of AR was studied once and revealed that oral roflumilast was effective as an anti-allergy therapy but was associated with significant adverse effects [10]. Further research on developing topical PDE4 inhibitors acting directly on the nasal mucosa is considered an effective future approach to minimize the associated adverse effects [10,35].

PDE4 Inhibitors in Bronchiectasis

Bronchiectasis is a chronic suppurative respiratory disease characterized by abnormal bronchial dilatation, chronic productive cough, and recurrent infective exacerbations [21]. Chronic neutrophilic airway inflammation is a key component of pathogenesis leading to persistent bronchial dilation and lung damage [20]. Some studies have attempted to identify the potential role of PDE4 inhibitors in the management of bronchiectasis because of their possibility to modulate neutrophil function, improve mucus and ciliary function, and the bronchodilator effect [6,20]. A phase II clinical trial using roflumilast in symptomatic bronchiectasis patients demonstrated improvement in health-related quality of life measured by the COPD assessment test score and the St. George’s Respiratory Questionnaire (SGRQ) but the findings were not statistically significant [20]. The first RCT done to identify the efficacy of roflumilast in bronchiectasis concluded that roflumilast did not significantly affect the rate of exacerbations or quality of life. However, there was an improvement in lung function (FEV1) compared to the placebo group [20]. Therefore, further research including long-term prospective clinical studies using more bronchiectasis patients will be helpful to fill the clinical gap identified in this group of patients.

PDE4 Inhibitors in Chronic Cough

Chronic cough, as a troublesome complaint of a significant proportion of the population, may occur due to many clinical pathologies [21]. Even though many anti-tussive medications are on the market, the limitation of effective therapeutic strategies may have contributed to its high burden [21]. The lack of mechanistic research to elucidate the cough mechanism was identified as a key issue in this field [21]. Transient receptor potential (TRP) ion channels are associated with a chronic cough in several diseases [36]. TRP ion channels modulate inflammation, smooth muscle tone, and sensory afferent activation in the airways, and they get activated by chemical stimuli, temperature changes, mechanical stress, and osmotic stress [36]. PDE inhibitors, which have anti-inflammatory and bronchodilator properties, also cause suppression of TRP channels [37]. Therefore, the use of PDE inhibitors in the management of chronic cough was proposed to be effective, and among them, selective PDE3, PDE4, and PDE5 inhibitors have demonstrated the most significant cough-suppressive effects [37]. Further clinical studies in this field will hopefully lead to new effective therapies for chronic cough.

PDE4 Inhibitors in Cystic Fibrosis

Cystic fibrosis (CF) is an autosomal recessive lethal genetic disorder caused by mutations in the CFTR gene [38]. CFTR anion channel regulates ion and water transport across multiple epithelia, and impairment of its function in respiratory epithelia disrupts airway innate defense mechanisms resulting in bacterial colonization, excessive inflammation, and tissue damage in the respiratory system [38,39]. In research data, roflumilast has been shown to activate CFTR ion channels in the respiratory epithelium of normal human cells [6]. The previous conclusion that PDE inhibitors are ineffective in restoring CFTR-dependent ion transport in cystic fibrosis mutated cells was challenged by a recent study that demonstrated selective PDE4 inhibitor-associated amplification in the CFTR correctors and/or CFTR potentiators [38]. The first evidence that PDE4 inhibition causes NETosis in cystic fibrosis was provided by recent in vivo and in vitro studies in CF-relevant models [40]. The pathogenic role of neutrophil-derived free DNA, which is released in the form of extracellular traps (NETs), causing impaired lung function in CF, was the target mechanism in this study, and PDE4 inhibitors demonstrated significant control of NETosis of neutrophils migrated into the lungs [40]. These recent clinical advances provide a platform for future researchers to design further studies on the effectiveness of PDE4 inhibitors in CF, which has been a troublesome clinical entity cared for by pediatricians.

Limitations

The search strategy for this systematic review was limited to four databases where only papers published in the English language in the last five years (2017-2022) were included. This study merely analyzed free full-text studies and thus may have precluded the inclusion of important studies. Therefore, a data gap within the study area is a possibility. While the number and quality of included studies were adequate, the majority of them were narrative reviews. A paucity of prospective studies that could be useful in determining the genuine relationship of PDE4 inhibitor therapy in other respiratory diseases such as CF, chronic cough, bronchiectasis, and allergic rhinitis was noted.



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People today are often unable to fully stretch their chest cavity when breathing due to poor posture. Patients with pulmonary obstruction, asthma, pulmonary fibrosis and other lung diseases experience shortness of breath, affecting their quality of life.

But lung rehabilitation exercises can strengthen the respiratory muscle groups, improve lung function, and relieve lung disease symptoms.

Diseases that Weaken Lung Function

There are two common types of lung diseases that can weaken lung function.

Obstructive pulmonary disease: The patient is unable to expel all the air from his or her lungs. Examples include lung injury or narrowing of the airways due to chronic obstructive pulmonary disease (COPD), asthma, or bronchiectasis.

Restrictive lung disease: There is a decrease in the total volume of air that the lungs are able to hold. For example, pulmonary fibrosis, interstitial lung disease, scoliosis, and obesity can result in stiffness of the lungs, tightness of the chest cavity, and weakness of the respiratory muscles.

The common symptoms of these two groups of patients are strained breathing and shortness of breath. Since whenever the patients move they wheeze, they try to avoid moving even more. This causes a vicious cycle, and their physical performance slowly declines.

In fact, exercise is the best rehabilitation treatment for lung disease. Lung rehabilitation exercises can improve the endurance and strength of the respiratory muscles and surrounding muscles, which in turn can enhance lung function and improve symptoms such as shortness of breath.

“For instance, for patients with pulmonary fibrosis, if their lung function is only three-fourths, pulmonary rehabilitation can improve the remaining function to four-fifths or five-sixths,” said Jen-Ting Lee, physiotherapist at the Department of Physical Medicine and Rehabilitation, Taipei Veterans General Hospital in Taiwan.

Epoch Times Photo

3 Major Lung Rehabilitation Exercises to Improve Lung Function

  1. Aerobic exercise

Aerobic exercise is a rhythmic movement of the large muscles in the entire body, which can improve muscle oxygen intake and cardiorespiratory function.

Calisthenics, walking, jogging, and cycling are all exercises that we can do frequently. The exercise duration should be at least 20 to 40 minutes at a time.

However, some lung disease patients cannot do exercises for 20 minutes at a time; they may do exercises multiple times a day, for the total exercise time to be added up to 20 minutes. Visible results will show after they do exercises three to five times a week for eight to 12 weeks.

  1. Strength training

Strength training can improve muscle endurance and muscle strength, thus enhancing respiration intensity and exercise tolerance.

Respiratory muscles are mainly composed of diaphragm muscles. However, strengthening the diaphragm muscles alone is not enough. If you want to breathe more easily during exercise, you also need to train other accessory respiratory muscles.

“These accessory respiratory muscles are all located in the upper body. So for patients with lung diseases, it’s important to train the upper body muscles,” said Lee.

You can use dumbbells, elastic bands, and other tools to increase the weight during exercise. The starting strength of the training is 50 percent to 60 percent of the one repetition maximum (1RM). 1RM is the maximum weight that a person can bear at one time. For example, if a person can’t lift a dumbbell of 20 pounds a second time after lifting it once with all his strength, then 20 pounds is the person’s 1RM. You can increase the strength gradually as the training progresses.

  1. Breathing exercises

Chest breathing, abdominal breathing, localized breathing, and full breathing can all train the lungs.

Speaking of breathing exercises, people first think of abdominal breathing. Abdominal breathing is indeed the best way of gas exchange, but some people are not suitable to do this exercise, such as patients with obstructive lung disease. If you don’t feel comfortable with abdominal breathing, it is equally effective to use other breathing methods.

Abdominal Breathing

Put your hands on your abdomen, inhale slowly through your nose, and feel your abdomen bulge. After inhaling to the fullest, exhale slowly through your mouth.

Epoch Times Photo
Lung rehabilitation exercise: abdominal breathing + round lip exhalation

 

“Many people do it wrong, because they push their abdominal muscles too hard,” Lee pointed out. When the body relaxes and allows the lungs to hold the air, the diaphragm will press down, and the stomach will naturally bulge.

People with obstructive lung disease are unable to exhale all the air in their lungs. They can use the “round lip exhalation” method, which is exhaling while puckering the lips. Round lip exhalation can increase positive pressure in the airways to help discharge the air.

Chest Breathing

Put your hands on your chest, slowly inhale through your nose, feeling the air filling your chest cavity, and your hands will slightly lift up along with your chest. After inhaling to the fullest, exhale slowly through your mouth.

Epoch Times Photo
Lung rehabilitation exercise: chest breathing

 

When breathing, pay attention to the relaxation of your shoulder and neck muscles, especially that your shoulders should not be raised.

Localized Breathing

Place both hands on your ribs, and your fingers will slightly part due to rib cage expansion as you breathe in to the fullest. It is better to do this exercise while lying down, because your shoulders are relaxed when lying down, so it is not easy to use the shoulder strength. And the effect will be better.

Epoch Times Photo
Lung rehabilitation exercise: localized breathing, with better results when lying down

 

The most important accessory respiratory muscles are the intercostal muscles. There are 12 ribs, with the first to sixth ribs being the upper ribs, and the seventh to twelfth ribs being the lower ribs.

When you breathe in to the fullest, the upper ribs expand forward to increase the space between the front and back of the chest cavity; and the lower ribs open upwards and to the sides to increase the left and right spaces of the chest cavity. As a result, the entire thorax opens up.

Localized breathing trains the intercostal muscles, allowing the thorax to expand more fully during breathing. This training is very important for patients with restrictive lung disease.

Full Breathing (i.e. Chest Breathing + Abdominal Breathing)

Place one hand on your chest and the other on your abdomen. When inhaling, your abdomen will bulge naturally, then deliberately inhale a little more, so that your chest will also bulge slightly. Then exhale. If you can’t expel all the air in your lungs, you can lower your head slightly to exhale all the air.

Epoch Times Photo
Lung rehabilitation exercise: full breathing

 

The way people normally breathe is full breathing. However, full breathing training is more intense than normal breathing.

When doing breathing exercises, you can combine them with thoracic exercises, to expand your chest cavity more fully.

The way to do this is to open your arms to the sides of your body when inhaling, and to fold your arms like holding a ball when exhaling. And then cross your arms in the lower front of your body, with your eyes looking towards your navel. Thoracic exercises are also beneficial for people with tight chests and poor breathing.

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AirPhysio is a breath training system designed to improve your breathing naturally.

The patented, doctor-approved device expands your airway through oscillating positive expiratory pressure (OPEP), helping you naturally improve your breathing over time. Many pulmonologists recommend the device to people with breathing difficulties.

Does AirPhysio live up to the hype? Should you buy AirPhysio? Keep reading to discover everything you need to know about AirPhysio and how it works.

About AirPhysio

AirPhysio is a breath training device sold online through GetAirPhysio.io.

Designed and patented in Australia, the device is a doctor-recommended, pulmonologist-approved way to improve your breathing. It’s an OPEP device that expands your airway, cleansing mucus and other contaminants from your airway and making it easier to breathe.

To use AirPhysio, just hold the device to your mouth, then breathe in and out as you normally would, pushing air through the system. As you breathe, AirPhysio creates positive pressure within your airway and lungs. This positive pressure dislodges mucus, allowing you to expel it from your body.

Many people develop breathing issues due to mucus buildup. Some people have medical conditions that lead to a greater buildup of mucus. AirPhysio claims to target and support these conditions in various ways, making it easier to breathe.

AirPhysio doesn’t just dislodge mucus from your airway and lungs; the device can also improve your lung strength and conditioning. Many people feel they can take deeper, stronger breaths after using AirPhysio. By clearing mucus from your airway, expanding your lungs, and strengthening your lungs, AirPhysio can improve your breathing in multiple ways.

You can buy AirPhysio through GetAirPhysio.io, where each device is priced at around $60.

How AirPhysio Works

AirPhysio is a patented device recommended by doctors to naturally improve your breathing. We’ll get more into the science of AirPhysio below. However, here are some of the crucial ways in which the device works:

Pulmonologist Recommended: AirPhysio is recommended by pulmonologists and other doctors as a way to naturally improve your breathing. Many pulmonologists specifically recommend AirPhysio as a way to improve your breathing by dislodging mucus from your airway.

Naturally Clear Mucus from Airways: The primary goal of AirPhysio is to use pressure to clear mucus from your airways. The device creates pressure that dislodges excess mucus build-up in your lungs, opening up blocked or semi-closed airways. After the mucus is dislodged, you can naturally expel the mucus from your body. AirPhysio helps you maintain optimal hygiene in your lungs while maintaining and restoring maximum lung capacity.

Feel It Working Instantly: AirPhysio doesn’t take days or weeks of use to work. Instead, you can feel the device working instantly. Most users feel a significant difference the first time they use AirPhysio. You can notice substantial changes overnight. Your lungs become noticeably clearer, making it easier to breathe. The more you use AirPhysio, the stronger and healthier your lungs will be.

Works for Respiratory Conditions: AirPhysio is a genuine medical device – not a home remedy or tool. It’s recommended by doctors for respiratory conditions. Hundreds of pulmonologists and other medical professionals recommend using AirPhysio to help with symptoms like asthma, atelectasis, emphysema, bronchiectasis, COPD, chronic bronchitis, and other respiratory issues.

Drug-Free, Natural, Safe, and Effective: Some doctors prescribe drugs to improve breathing. Other doctors recommend surgery or other treatments. AirPhysio works differently. It’s a natural, safe, effective, and 100% drug-free way to improve your breathing. You’re clearing your airways of mucus, allowing you to naturally improve your normal breathing habits.

Portable and Easy to Use: You can bring AirPhysio with you anywhere you go. The device is easy to use on-the-go, while traveling, or at work. Just remove AirPhysio from your pocket, blow into the device for a few seconds, then put it away. It’s that easy. It’s as discreet – if not more discreet – than asthma puffers and other treatments.

Medical-Grade Without a Prescription: AirPhysio is made from high-quality, medical-grade materials. It’s also 100% drug-free. You can buy one or more AirPhysio units online without a prescription.

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The Science Behind AirPhysio

AirPhysio dislodges mucus from your airway using oscillating positive expiratory pressure, or OPEP. You can find other OPEP machines that do a similar job. However, AirPhysio has a patented design and is recommended by pulmonologists specifically to improve breathing.

You start by holding the AirPhysio mouthpiece to your mouth. Then, breathe out. As you exhale, AirPhysio creates positive pressure in your lungs. This positive pressure forces mucus to come away from the walls of your airway, allowing you to remove the mucus from your body naturally (by swallowing or coughing). That means less mucus coating your airways and lungs – and easier breathing for you.

Breathing issues aren’t always linked to mucus in your airways. However, many breathing problems force more mucus to coat your airway. It’s a symptom of a condition. AirPhysio could help you target this symptom, clearing your airway to allow for easier breathing.

When mucus lines your airway, it makes it difficult to breathe. AirPhysio dislodges this mucus naturally: it creates pressure that forces mucus away from your airway, allowing your body to expel the mucus naturally. You get all of the benefits of a decongestant or similar drug – but without taking any medication.

As mentioned above, you can feel AirPhysio working instantly. After a few seconds of blowing through AirPhysio, you should start to notice the effects of pressure. After a few breaths in and out through the device, mucus has been dislodged from your airway.

Pulmonologists and other doctors recommend AirPhysio for various respiratory conditions. According to the official website, hundreds of doctors and pulmonologists around the world recommend AirPhysio for COPD, atelectasis, asthma, bronchiectasis, emphysema, chronic bronchitis, and related conditions.

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AirPhysio’s Patented Design

AirPhysio is a patented device with a straightforward design. The device uses simple physics to create positive pressure in your lungs and airway. Because it’s patented, AirPhysio has been verified to have a unique design compared to other OPEP systems available today.

The three core components of AirPhysio include:

  1. Protective cover
  2. Steel ball
  3. Circular cone

You remove AirPhysio from the protective cover, then breathe through the mouthpiece. As you breathe, your air encounters the steel ball and circular cone. The ball and cone create air resistance, leading to positive pressure in your lungs and airway. This pressure removes mucus from your lungs and airway, helping you manage breathing conditions without drugs or surgery.

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How OPEP Devices Work

AirPhysio is part of a family of devices known as OPEP devices. They’re also known as lung training systems or breathing trainers, among other names.

OPEP devices all work in a similar way. By definition, OPEP devices use oscillating positive expiratory pressure (OPEP) to improve your breathing. This pressure dislodges mucus and other contaminants from your airway, making it easier to breathe.

As you use AirPhysio and other OPEP devices, you may feel vibrations or pulses loosen mucus along the walls. These vibrations are the ‘oscillating’ part of the oscillating positive expiratory pressure. The oscillations force the mucus away from the walls. Normal air doesn’t oscillate as it travels through your airway. By oscillating this air, OPEP devices dislodge mucus and other contaminants.

Most OPEP devices create oscillation using a valve or similar system. Valves switch between high and low resistance, creating positive pressure within your lungs and airway.

This positive pressure works similar to a balloon. It holds your airways and lungs open – just like it would when blowing up a balloon. As your lungs and airways expand and vibrate, it dislodges mucus

Some OPEP devices let you adjust the resistance based on your comfort. As your lungs become stronger and clearer, you can increase the resistance for added effectiveness. When starting out, you may want to keep it on the lowest setting.

OPEP devices are priced between $30 and $200. You can buy them online or at any pharmacy. High-end devices use complex valves to create oscillation. Cheaper devices use physical systems – like the cone and ball within AirPhysio – to create those same oscillations.

Overall, AirPhysio claims to give you the effectiveness of a higher-end system without the high price tag. You get all of the benefits of an OPEP device without spending a fortune.

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What to Expect After Using AirPhysio: Scientific Evidence for AirPhysio

AirPhysio is a patented, award-winning device approved by doctors and pulmonologists to improve breathing. Some doctors recommend AirPhysio for specific breathing conditions. Others recommend it to anyone who wants to improve lung capacity or boost their ability to get a full breath.

The makers of AirPhysio claim that mucus clearance problems can lead to a loss of 11mL (1 shot glass) of lung function every year. For every year you go without clearing mucus from your lungs, you lose a small portion of your lung capacity. When left untreated over time, this can create serious breathing difficulties.

Mucus buildup can be a symptom of a condition. Or, it could occur naturally due to lifestyle factors or dietary reasons. As mucus builds up, it can make it harder to breathe.

Science tells us that AirPhysio and other OPEP devices can be effective for the following conditions:

  • Asthma
  • Atelectasis
  • Bronchiectasis
  • COPD
  • Emphysema
  • Chronic bronchitis

AirPhysio is also marketed to smokers and the elderly. Smokers and the elderly may have breathing issues related to mucus in their lungs.

Others have shortness of breath for other reasons. You might struggle to fill your lungs with every breath. AirPhysio could improve your lung capacity in various ways.

To understand how AirPhysio works, it helps to understand the conditions it’s designed to help. Atelectasis is a complete or partial collapse of the entire lung or a lobe of the lung. Tiny air sacs within your lung deflate and fill with alveolar fluid, leading to atelectasis. Some people develop atelectasis after surgery. Others experience atelectasis after a chest injury or a lung tumor. Atelectasis is also linked to breathing in foreign objects and cystic fibrosis, among other factors. Your doctor can diagnose atelectasis via a CT scan, thorax ultrasound, bronchoscopy, or oximetry.

Breathing issues can lead to hypoxemia. If your body isn’t getting enough oxygen, then you develop hypoxemia, which is a fancy way to say you have low blood oxygen levels. When you blood is low on oxygen, it’s difficult for your lungs to get oxygen to the air sacs, disrupting your normal breathing process. Hypoxemia can be difficult to detect, but it could create more serious symptoms. Hypoxemia is linked with cognitive issues, fatigue, general feelings of unwellness, and other symptoms.

Doctors recommend different treatments for atelectasis based on the severity of your condition. Generally, deep breathing exercises are part of any atelectasis treatment plan. Also known as incentive spirometry, deep breathing exercises can train your body to suck in more oxygen from each breath. Some doctors also recommend breath training devices – like AirPhysio and similar machines.

More severe cases of atelectasis may require surgery. Doctors may recommend a bronchoscopy, where they siphon mucus out of the airway using a flexible tube.

With AirPhysio, you could manage symptoms of atelectasis and other breathing issues by improving your body’s natural breathing. The device is recommended by doctors and hospitals worldwide for atelectasis and other breathing problems.

AirPhysio Customer Reviews

The makers of AirPhysio have sold over $1.2 million of product since launch. Most customers agree that AirPhysio works as advertised to dislodge mucus from the lungs. Some of the best endorsements of AirPhysio come from doctors and pulmonologists.

Here are some of the reviews for AirPhysio as shared on the official website:

One woman was skeptical about the benefits of AirPhysio because she had suffered from asthma serious enough to require steroids. Although steroids helped her asthma, she found AirPhysio really helped to clear her airways – all without the use of drugs.

Another woman described AirPhysio as a “miracle device” because of its effects on mucus in her lungs and airways. She claims that after using AirPhysio just once, she was coughing up junk in her lungs. She had suffered from breathing issues since a three-week bout with pneumonia, and she found that AirPhysio helped.

One registered nurse (RN) cited on the AirPhysio sales page recommends using AirPhysio for pneumonia and pleurisy following brain surgery. That RN also recommends AirPhysio to athletes who want to improve lung capacity. She has witnessed the effects of AirPhysio firsthand, and she believes it can help people improve breathing for different reasons and in different situations.

Other users report feeling short-term and long-term benefits associated with AirPhysio. Most users report feeling immediate changes after using AirPhysio for the first time. Most users also experience greater benefits after weeks of use.

Some users stop taking drugs or following treatment programs after using AirPhysio successfully. One user claims she no longer takes albuterol, uses a nebulizer, or takes any steroids to manage her breathing conditions (she has COPD and chronic bronchitis). Instead, she only uses AirPhysio.

Overall, AirPhysio has strong reviews from nurses, doctors, pulmonologists, and ordinary people. Some people use AirPhysio for specific breathing conditions, while others use AirPhysio simply to improve their lung capacity.

AirPhysio Pricing

AirPhysio is priced at $60 per unit when purchased through GetAirPhysio.io, with discounts available when ordering 3 or 5 units.

Here’s how pricing breaks down at GetAirPhysio.io:

  • 1 Unit: $59.99 + $5.99 Shipping
  • 3 Units: $119.98 + Free US Shipping
  • 5 Units: $179.97 + Free US Shipping

You can use each AirPhysio unit an unlimited number of times. It doesn’t require batteries or electronics to run. It uses physical systems to create resistance. Each AirPhysio is designed for one person to use.

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AirPhysio Refunds

GetAirPhysio.io offers refunds on purchases within 30 days. To be eligible for a return, your item must be returned in its original packaging. You also need to provide proof of purchase (like your order number).

You can request a refund within 30 days of your original purchase date. You will receive a refund minus original shipping costs.

To initiate the refund process, email [email protected]

AirPhysio Warranty

AirPhysio is backed by a one year warranty. All purchases are protected for one year from your original purchase date against manufacturer’s defects.

Who Made AirPhysio

AirPhysio was developed by an Australian team of inventors. The product is made in Australia and created by an Australia-owned company. It’s also patented and ward winning. The team won Australia’s Start-Up Business of the Year award in 2017.

To sell AirPhysio online, the inventors partnered with a third-party ecommerce company named GiddyUp. GiddyUp operates GetAirPhysio.io. When you buy AirPhysio through GetAirPhysio.io, you’re buying directly from the original inventors and supporting the original inventors.

All customer service queries can be directed to the original inventors of AirPhysio via the following:

  • Email: [email protected]
  • Phone: 1300 723 110
  • Mailing Address: Shop 3, 47 Tweed Heads Road, Cabarita Beach, NSW 2488

Conclusion

AirPhysio is an OPEP breath training device available through GetAirPhysio.io. Priced at $60 per unit, AirPhysio dislodges mucus from your airways while strengthening your lungs, helping to naturally improve your breathing.

AirPhysio is recommended by hundreds of pulmonologists and doctors around the world as a treatment for breathing problems. The device is marketed as a way to treat and prevent respiratory complications.

AirPhysio is available for purchase today through GetAirPhysio.io.

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Bronchiectasis and chronic obstructive pulmonary disease (COPD) are two chronic conditions that involve damage to the lungs.

The causes and treatments for each differ. In some instances, COPD may cause bronchiectasis.

Read on to learn about the differences and similarities between bronchiectasis and COPD and how each condition is treated.

Bronchiectasis is a progressive lung condition caused by damage to bronchi (large air passages) in the lungs. With bronchiectasis, the walls of the bronchi become thickened from ongoing inflammation or infection.

People with this condition cough up large amounts of mucus, especially during flareups. Flareups of bronchiectasis are referred to as exacerbations. During an exacerbation, you will also find it harder to breathe.

Bronchi are designed to enable free breathing by letting air enter the lungs. Bronchiectasis occurs when the bronchi in the lungs become chronically inflamed and thickened. Over time, the thickening of the bronchial walls and subsequent scarring make it hard to move mucus out of the lungs. Recurring infections also become more likely.

Bronchiectasis occurs most often in people ages 75 and over. However, you can get this condition at any age. Having cystic fibrosis is a risk factor.

The underlying causes of bronchiectasis are not always known. However, this condition is often caused by other health conditions and infections that damage the lungs. These include:

People with bronchiectasis can live their usual lives, but exacerbation periods may be challenging. Diagnosis and treatment are essential for the best outcomes.

Chronic obstructive pulmonary disease (COPD) is an umbrella term for a group of progressive lung diseases that include chronic bronchitis and emphysema. People with COPD may have both of these conditions simultaneously.

COPD is a serious, chronic disease that progressively worsens over time. People over age 40 are at the highest risk, especially if they smoke. The use of tobacco products, such as cigarettes, is the most common cause of this condition.

COPD causes inflammation and thickening of bronchi in the lungs. It can also cause damage to lung tissue and the air sacs in the lungs. This results in difficulty breathing in oxygen, plus difficulty breathing out carbon dioxide. Carbon dioxide is a waste product of cells that are produced during respiration.

According to the American Lung Association, COPD can cause long-term disability and early death, especially if untreated.

People with COPD may have trouble breathing every day or almost every day. Flareups with more intense symptoms can also occur. COPD symptoms worsen over time and may eventually include:

  • wheezing
  • shortness of breath after mild exertion
  • tightness in the chest
  • chronic cough that may or may not produce mucus
  • swollen legs and feet
  • extreme fatigue

Bronchiectasis and COPD are not the same condition. However, they’re both progressive lung diseases. Both conditions can make it hard to intake oxygen and release air from the lungs. Other shared symptoms include breathlessness, wheezing, and coughing.

Emphysema, a type of COPD, is different from bronchiectasis. For people with emphysema, damage occurs to the walls between air sacs in the lungs, making the walls less stretchy and less able to fill up with air. Bronchiectasis doesn’t cause damage to air sacs.

Chronic bronchitis, another type of COPD, is also different from bronchiectasis. But, because it causes inflammation and narrowing of the bronchia, COPD is sometimes confused with bronchiectasis. Symptom overlap also causes people to confuse the two.

Bronchiectasis and COPD can occur together. This is referred to as bronchiectasis-chronic obstructive pulmonary disease overlap syndrome (BCOS). Some studies indicate that people with BCOS have poorer outcomes than people with only one condition.

One study found that people with BCOS had more incidents of acute respiratory distress than people who had COPD without bronchiectasis.

Since they’re both chronic lung conditions, bronchiectasis and COPD have many symptoms in common. These include:

  • chronic cough that produces mucus
  • wheezing
  • fatigue
  • shortness of breath
  • respiratory infections

While COPD and bronchiectasis are both chronic lung diseases that can make it difficult to breathe, they’re different. Here are the main ways the two conditions are different:

Causes

The leading cause of COPD is smoking cigarettes. Exposure to secondhand or thirdhand cigarette smoke as well as exposure to pollution and poor air quality can also cause COPD.

Bronchiectasis is usually caused by other health conditions a person has.

Symptoms

There are a few different symptoms between the two.

Bronchiectasis can cause:

  • clubbing (thickened skin under toenails or fingernails)
  • hemoptysis (coughing up blood or a mucus-blood mixture)

COPD can cause:

Diagnosis

Another difference between COPD and bronchiectasis is how they’re diagnosed.

COPD is a physiologic diagnosis.

  • COPD is diagnosed based on an assessment of how your lungs actually function. COPD is diagnosed through a test called spirometry, which tests how well your lungs function by measuring airflow in and out of your lungs.

Bronchiectasis is a structural diagnosis.

  • Bronchiectasis is diagnosed based on how your airway, specifically the tubes that lead into your lungs called bronchi, appears on images from a CT scan. In people who have bronchiectasis, the bronchi are dilated and thickened, which narrows the airway.

Treatment for bronchiectasis is designed to prevent lung infections and reduce or prevent exacerbations (flareups). These treatment options include:

  • Antibiotics. Antibiotics are a common, first-line treatment. Usually, antibiotics are taken orally. If your symptoms are severe, your doctor may recommend intravenous antibiotics. These are given via injection.
  • Mucus-thinning medications. Mucus-thinning medications may help reduce and remove mucus. You usually inhale these medications through a nebulizer. For some people, a decongestant may also help prevent or reduce congestion.
  • Handheld airway clearance devices. Handheld airway clearance devices that you exhale into may also help break up mucus.
  • Chest physiotherapy (chest physical therapy). These therapeutic techniques may be used to loosen mucus from the lungs. To do chest physiotherapy, a physical therapist will use certain techniques, such as clapping on your chest. Electronic chest clappers you can use at home are also available that mimic the hand motions used by physical therapists.
  • Smoking cessation. If you smoke, your doctor will recommend ways that may help you quit smoking.

If you smoke, stopping will be an important part of COPD treatment. Smoking cessation can help slow the progression of your disease. Talk with your doctor about smoking cessation aids, so you can choose the best type for you.

Other treatment options for people with COPD may include:

Medications

Medications like inhaled bronchodilators and corticosteroids are commonly prescribed medications for COPD:

  • bronchodilators widen the airways and relax lung muscles, making it easier to breathe
  • corticosteroids reduce inflammation and swelling

Based on your symptoms and the severity of your disease, your doctor may prescribe a short-acting or long-acting bronchodilator for you to use. If your symptoms are severe, inhaled steroids you breathe in along with a bronchodilator may also be prescribed.

Oxygen therapy

If your blood oxygen levels are low, oxygen therapy may be used at home or in a medical setting. Oxygen therapy delivers oxygen to your respiratory system so you can breathe better. It may be delivered through a face mask or tube.

Pulmonary rehabilitation

A supervised pulmonary rehabilitation program will be recommended as part of treatment. Pulmonary rehabilitation may last for weeks or months. It’s designed to teach you COPD management skills that will help you live a healthier life. These include:

Surgery

If your disease is severe and doesn’t respond to medication, surgery may be an option. There are several types of surgery:

  • Bullectomy. A bullectomy is done to remove large bullae (air spaces) caused by destroyed air sacs in the lungs.
  • One-way endobronchial valve implantation. During one-way endobronchial valve implantation, a valve is inserted into a bronchial tube. The valve helps air leave the lung but not re-enter.
  • Lung volume reduction surgery. During lung volume reduction surgery damaged lung tissue is removed.
  • Lung transplant. In a lung transplant, a diseased lung is removed and replaced with a healthy one.

Bronchiectasis and chronic obstructive pulmonary disease (COPD) are two progressive lung diseases. Even though they share some symptoms, they’re not the same condition.

The main cause of COPD is smoking cigarettes. Bronchiectasis is usually caused by other health conditions. Both conditions are chronic but can be treated with medication, lifestyle changes, and other strategies.

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Dr Ranj Singh on the Strictly Come Dancing red carpet 2019

Pictures: PA

Dr Ranj Singh on the Strictly Come Dancing red carpet 2019 Pictures: PA

The TV medic opens up about struggling with work pressures, brain fog and why having a night-time routine is so important. By Lauren Taylor.

Paediatric consultant Dr Ranj Singh is usually the one handing out health advice on TV, but health professionals are notorious for not prioritising their own wellbeing, he says.

"I think we're all really guilty of being great at looking after others and not being necessarily the best at looking after ourselves. And that's something that really needs to change," says the 42-year-old, best known for ITV's Dr Ranj: On Call and Cbeebies' Get Well Soon.

Alongside his TV work, he's a part-time NHS consultant in children's A&E - "A very rewarding job," he says, "I love doing it and I'm very lucky to be able to do it, but it can be stressful."

Having suffered from burnout five years ago, he knows the dangers of pushing himself too far at work. "That was really difficult for me to admit and it was really difficult for me to take a step back at that point," says the former Strictly Come Dancing contestant.

"Initially, it feels just like stress, but then it obviously progresses and starts to affect your life a lot more significantly. I realised that I wasn't able to give my job 100% and I was really, really struggling. For me, time management became a real problem - and it's never been a problem for me before. I had to stand back and think, 'hang on a second, something's not right' - I'd hit that burnout point."

Thankfully, he had good senior support at work and was able to take time off to get back on his feet. "The best thing for me to do was give myself some space and breathing room to process. But I'm glad I did, because it really, really helped."

But, he says, there's "too much shame and stigma attached [to burnout] - particularly for health professionals.... Sometimes we're the least likely people to ask for help".

So, taking breaks has become key to Singh's wellness routine - on top of "a normal balanced diet, as much activity as I can, and I look after my sleep - those three things are core to everything".

But "self care for me isn't just about the things I do to myself, it's the environment in which I exist" - and that's something not enough of us pay attention to, he says.

A new study of 2,000 people by Breville found that 46% had never heard of indoor air pollution - yet it can be harmful to our health, says Singh. "Indoor air, the air that's inside our homes, can sometimes be three and a half times more polluted than outdoor air."

Lighting candles, using a wood-burning stove and chemical cleaning products can all contribute to poor air quality - and can generate gasses that can exacerbate underlying medical problems like, asthma, bronchiectasis or wheezing.

"Poor indoor air quality also contributes to long-term conditions like heart disease and stroke, and can even increase your risk of those sorts of things. So, it's not something we can ignore," he explains.

Air quality is obviously important in the fight against airborne infections like Covid, too. Singh was diagnosed with long Covid last summer and although he's "coming through the other end of it" he's suffered with brain fog as a result.

"The way it manifests for me - and it's different for everybody - is that my memory isn't as good, my concentration gets affected and any kind of higher or executive thought for me is more difficult. That's why work became particularly tricky - and then it led to an anxiety, which I'd never really experienced."

He's also found lasting limitations in the amount of exercise he can do; "I might get tired or breathless quite quickly, but that's getting better. I have to be mindful I don't push myself too hard, too quick - when it comes to long Covid, that can actually set you back and delay your recovery.

"I try to pace myself as best I can, I'm a 'yes' person, so I like to take every opportunity. But one of the big things I've learned particularly through long Covid and brain fog is to say 'no' to things and to be OK with saying no - not because I want to, but because I can't.

"I think a lot of us struggle to admit that actually we are only human - we can only do so much and and sometimes pacing yourself and slowing down is just as important as achieving things."

Looking after his mental health has been "an active learning process" (he opened up to Attitude UK about the "lowest point in his life" and feeling like "a very sad, destructive, angry mess" after breaking up with his wife in 2009 and coming out).

"For me, routine is really important. It's about being as productive as I can be within my means and within my energy levels, also taking breaks and giving myself space to breathe. [Then] leaning on and talking to the people around me when I need.

"In the evenings, it's all about slowing down. Not doing things that are too stimulating, having a bedtime routine. I'm one of these people who has to relax, have a shower, maybe watch something relaxing before going to bed.

"The world might be 24/7 but we can't be."

Men, particularly, don't always dedicate enough time for their own self-care, he agrees. "I don't think men have been given permission! Sadly, the traditional narratives have been that as a man, you have to pull your socks up, get on with it and not complain; be the leader, be the strong one, don't show your emotions - that narrative is really harmful, really toxic.

"I think it's important for us to give men and young boys permission to express themselves to talk, especially when they're in need of help. And also just normalise the fact that boys feel too - men feel as well."

Breville has launched its new 360 air purifier range to reduce air pollution at home. Available on Amazon.

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We are delighted to announce the 8th Biennial Seminar in Paediatric Respiratory Medicine at the Sydney Children’s Hospital, Randwick.

For the first time, we will also be introducing our interactive short course scheduled for 1/2 day on 24 September. The short course offers three engaging modules with practical workshops to provide you with insights, tools and updates on Spirometry (Lung Function), Chest Physiotherapy techniques and Asthma Inhaler Devices.

The seminar and short course cover face to face presentations, practical activities, engaging discussions with industry leaders, and online course materials.

Over a period of 1 ½ days, you will have the opportunity to join thought-provoking debates and deep dive discussions from some of the world’s brightest minds in paediatric respiratory medicine!

So, mark your calendars and register to join us! We look forward to seeing you there!

About the seminar

The seminar aims to give you insights, practical tools and updates on best practice in paediatric respiratory medicine on a day-to-day basis.

Brought to you by UNSW Medicine & Health and the Sydney Children's Hospitals Network (SCHN), the seminar offers a series of interactive face to face presentations, engaging discussions, practical short course modules, and online course materials by leading experts in children's respiratory medicine in Australia and New Zealand.

Who should attend this seminar?

Paediatricians, GPs, junior doctors, nursing staff, allied health professionals and other interested health workers who are involved in the care of children with acute and chronic respiratory conditions.

About the short course

The short course is a collaboration between the UNSW Medicine & Health and the Sydney Children’s Hospitals Network (SCHN). Brief descriptions of the 3 modules are below:

  1. Spirometry (Lung Function): covering how do you interpret lung function (good quality vs uninterpretable lung function), how to approach a breathless child - exploring the techniques of exhaled nitric oxide (FeNO), provocation test such as mannitol challenge, and cardiopulmonary exercise testing (CPET).
  2. Chest Physiotherapy: covering who to refer and who doesn’t need referral (inpatient vs outpatient), what improvement you can expect from chest physiotherapy, new vs old techniques.
  3. Asthma Inhaler Devices: covering why do we need asthma education and how to provide education, advice on improving breathing including indoor air quality, house dust mite minimisation, how to provide a green asthma management plan (including new vs old devices and techniques).

Delegates are expected to attend the short course on 24 September which will be delivered sequentially one after another. An assessment consisting of 25 multiple choice questions (MCQs) will be available for credentialing.

What are the course credentials?

Upon successful completion of the assessment, you will be issued with a UNSW Medicine & Health verifiable credential badge. The credential provides formal recognition of professional development and reflects 1.5 days of learning inclusive of the 1 day seminar and 1/2 day short course.

The 1.5 days of learning and verifiable credential may be counted towards your continuing professional development (CPD). Please check with your college as the credential provides documentary evidence which may substantite activities claimed under your college program.

 

Q&A questions

Please feel free to send your questions ahead of time to shortcourses.health@unsw.edu.au.

Event registration

Early registration is recommended as places are limited.

Registration Price (GST inc.) For online price use discount code at checkout
Seminar & Short Course (in person) $500.00  
Seminar & Short Course (online) $450.00 PRMSONLINE

Inclusions

Price is inclusive of 1 ½ day seminar covering deep insights, practical tools and updates on best practice in paediatric respiratory medicine on a day-to-day basis, our short course (in person and online), professional learning and development materials, online learning resources, evidence-based research, practical tools and techniques, courses completion assessment, digital badging, and networking.

Morning tea, lunch and afternoon tea will be provided on Day 1 and morning tea will be provided on Day 2. All are covered in the price for attending the seminar in person.

Seminar program: Friday 23 September (full day)

Time Topic Speakers
8:00 - 8:50 Registration  
8:50 - 9:00 Welcome and Introduction Cathryn Cox, Chief Executive, SCHN
Session 1: Upper Airways
9:00 - 9:30 I can’t breathe - causes of shortness of breath on exercise dyspnoea Professor Hiran Selvadurai
9:30 - 10:00 The importance of sinuses in respiratiry health Dr Catherine Banks
10:00 - 10:30 Screening and managing children with obstructive sleep disordered breathing Dr Mimi Lu
10:30 - 11.00  Morning Tea  
Session 2: Respiratory Hot Topics
11:00 - 11.30 Improving asthma outcomes Dr Nusrat Homaira 
11.30 - 12:00 Virtual care in children with chronic respiratory condition Michael Doumit
12:00 - 12.30 Latest advances in therapeutics for respiratory disease in CF and SMA Dr Sandra Chuang
12:30 - 13:00 To eat or not eat peanut Dr Brynn Wainstein
13:00 - 14:00 Lunch  
Session 3: Latest Guidelines
14:00 - 14:30 Update on Tracheo-oesophageal fistula management guideline Dr Yvonne Belessis
14:30 - 15:00 Improving outcomes for non-CF bronchiectasis Dr Bernadette Prentice
15:00 - 15:30 Respiratory guidelines for Cerebral Palsy Prof Adam Jaffe
15:30 - 15:50 Afternoon Tea  
Session 4: Challenges in breathing
15:50 - 16:20 3 challenging cases Dr Louisa Owens
16:20 - 16:50 Promoting health in adolescents: vaping and tobacco control Alecia Brooks
16:50 - 17:20 John Beveridge Oration – Lessons learnt from the health system in COVID A/Prof Lucy Morgan
17:20 - 17:30 Program Evaluation QR code here

Short course program: Saturday 24 September (½ day)

Time Topic Presenters
8:30 - 9:00 Registration  
9:00 - 9:40

Chest Physiotherapy: covering who to refer and who doesn’t need referral (inpatient vs outpatient), what improvement you can expect from chest physiotherapy, new vs old techniques

Michael Doumit
9:40 - 10:20

Asthma Inhaler Devices: covering why do we need asthma education and how to provide education, advice on improving breathing including indoor air quality, house dust mite minimisation, how to provide a green asthma management plan (including new vs old devices and techniques)

Melinda Gray
10:20 - 10:50 Morning tea  
10:50 - 11:30

Spirometry (Lung Function): covering how do you interpret lung function (good quality vs uninterpretable lung function), how to approach a breathless child - exploring the techniques of exhaled nitric oxide (FeNO), provocation test such as mannitol challenge, and cardiopulmonary exercise testing (CPET)

Jamie McBride
11:30 - 12:00pm Assessment: consisting of 25 multiple choice questions (MCQs) Dr Sandra Chuang
12:00 - 12:30pm Q&A and Closure Dr Sandra Chuang

Speakers & presenters

Listed in order of speaker and presenter appearance.

Day 1

 
Cathryn Cox PSM – Chief Executive, Sydney Children’s Hospitals Network (SCHN)
Professor Hiran Selvadurai – Head of Respiratory Medicine Department, The Children’s Hospital at Westmead
Dr Catherine Banks –  Ear, Nose and Throat Surgeon, Sydney Children’s Hospital Randwick and Prince of Wales Hospital
Dr Mimi Lu – Respiratory and Sleep Physician, Sydney Children’s Hospital Randwick and Children’s Hospital Westmead, Woolcock Clinic
Dr Nusrat Homaira – Respiratory Epidemiologist, Early Career Fellow of National Health and Medicla Research Council, Senior Lecturer with Discipline of Paediatrics UNSW, honorary research scientist SCH Randwick
Michael Doumit – Senior Physiotherapist, SCH Randwick, Conjoint Associate Lecturer Discipline of Paediatrics UNSW, Lecturer in Physiotherapy, Department of Health Sciences Macquarie University
Dr Sandra Chuang – Respiratory Clinical Academic SCH Randwick, Lecturer Discipline of Paediatrics UNSW
Brynn Wainstein – Paediatric Immunologist and Allergist SCH Randwick, Conjoint Senior Lecturer Discipline of Paediatrics UNSW, President of the Australasian Society of Clinical Immunology and Allergy (ASCIA)
Dr Yvonne Belessis – Respiratory Physician SCH Randwick, Conjoint Senior Lecturer Discipline of Paediatrics SCH
Dr Bernadette Prentice – Respiratory Physician, SCH Randwick
Prof Adam Jaffe – Respiratory Clinical Academic SCH Randwick, John Beveridge Chair of Paediatrics
Dr Louisa Owens – Head of Respiratory Medicine Department, SCH Randwick; Conjoint Lecturer Discipline of Paediatrics UNSW
Alecia Brooks – Manager, Tobacco Control, Cancer Council NSW
A/Prof Lucy Morgan – Clinical Associate Professor, Concord Clinical School

Day 2

 
Michael Doumit – Senior Physiotherapist, SCH Randwick, Conjoint Associate Lecturer Discipline of Paediatrics UNSW, Lecturer in Physiotherapy, Department of Health Sciences Macquarie University
Ms Melinda Gray – Respiratory Clinical Nurse Consultant, Department of Respiratory Medicine, Sydney Children’s Hospital Randwick
Jamie McBride – Senior Respiratory Scientist, SCH Randwick

Venue & transport

Venue

John Beveridge Lecture Theatre, Level 1
Sydney Children’s Hospital
High St, Randwick NSW 2031

Map

Parking

Street parking is very limited. All-day parking is available at the Prince of Wales Hospital Car Park, via Barker St, Randwick (Maximum daily rate: $31.20).

Drop-off zone

There is a drop-off zone in the driveway of the Sydney Children’s Hospital on High St, Randwick.

Public Transport

For timetable information call the Transport Infoline on 131500 or see www.transportnsw.info

Cancellations & Refunds

Cancellation must be provided in writing to UNSW in which case the following terms and conditions apply:

  • If written notice is received by UNSW more than 10 working days prior to the seminar commencement date, 80% of the fees and charges will be refunded.
  • If written notice is received by UNSW less than 10 working days prior to the seminar commencement date, 50% of the fees and charges will be refunded.
  • No refund of the fees and charges will be made if written notice is received on or after the seminar commencement date or in the case of non-attendance at the seminar.

Accommodation

Delegates are advised to make their own arrangements for accommodation, if required.

Seminar, short course and course materials

Seminar, short course and course materials will be available in the UNSW Medicine & Health Canvas learning management system.  

Liability

The program is correct at the time of issuing. However, the organisers reserve the right to alter the program without notice due to unforeseen circumstances. The seminar organisers accept no responsibility for any loss incurred by registrants resulting from their attendance at the seminar.

The Inaugural John Beveridge Lecture

The John Beveridge Lecture recognises the life, contribution and commitment of Professor John Beveridge, to the health and welfare of children.

John Beveridge was the Foundation Professor of Paediatrics at the University of NSW and the Director of the Prince of Wales Children’s Hospital (now the Sydney Children’s Hospital, Randwick) from its inception in 1962 until 1991.

During his early career, he realised that paediatrics was his passion, and he is remembered for his high standards of service and care. Professor Beveridge was a strong, passionate and determined advocate for the Hospital specifically, and for children’s health more widely.

His clinical interest in respiratory conditions, like cystic fibrosis, provides a poignant connection to the respiratory presentations which will be delivered at this forum.

Reach us for further information about this seminar and the short course. We continuously improve our short courses, education and training, seminars and bespoke programs to reflect the needs of our learners and their employers. If you are interested in connecting with us to explore bespoke program for your organisation or team, please contact us.

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Background: Most of the acute exacerbations of chronic obstructive pulmonary disease (COPD) are due to infections, mostly due to bacteria and viruses. There is a need to study the outcome of microbe-induced airway inflammation.

Materials and methods: It is an observational follow-up study from the pulmonary medicine department of Kalinga Institute of Medical Sciences with the participation of the Regional Medical Research Center, Bhubaneswar, from October 2018 to February 2022. Patients who were admitted with acute exacerbation of COPD and treated as per GOLD (Global Initiative for Chronic Obstructive Lung Disease) 2021 guidelines were included in the study. Those patients in the severe category, who had clinically recovered, had undergone pulmonary physiotherapy, were on prescribed medications and home oxygen therapy after discharge, were followed up every three months by telephone calls. Any exacerbation, clinical stability, or mortality information was recorded.

Results: Out of 197 cases, the majority were elderly, males, smokers, and belonged to urban areas; in total, 102 (51.8%) microbes were isolated as etiological agents of infective exacerbation in which 19.79% were viruses and 23.35% were bacteria, while coinfection was found in 8.62% cases. Among the viruses, rhinovirus, influenza virus, and respiratory syncytial virus were the major isolates. Among the bacteria, mostly gram-negative organisms such as Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas aeruginosa were isolated. Readmission was more among patients with coinfection.

Conclusion: Acute exacerbation of COPD was mostly seen in males in the age group of 61-80 years. Rhinovirus and influenza A virus were the two most common viral isolates, and among the bacterial isolates, Acinetobacter baumannii and Klebsiella pneumoniae were predominantly detected. Poor clinical outcomes were noticed more among the coinfection group.

Introduction

Worldwide, COPD is one of the major causes of illness and the sixth highest cause of death. According to research on the Global Burden of Diseases in 2017, it contributed to 50% of all chronic respiratory diseases. It is currently the third leading cause of death worldwide, accounting for nearly 3.23 million deaths, with nearly 80% of deaths occurring in the middle- and low-income countries, and is expected to rise from the 12th leading cause of disability-adjusted life-years (DALYs) in 1990 to the fifth leading cause in 2020 [1,2].

Acute exacerbations of COPD are significant events in the course of illness because they have a negative influence on health status, hospitalization rate, and disease progression. It is believed that respiratory infections are an important risk factor for COPD exacerbations, with viruses accounting for 22%-64% [3]. The increased exposure to viruses in winter has been correlated to an increase in the frequency of exacerbations in winter in some areas of the world [4]. Co-infections have also been linked to an increase in the severity of COPD exacerbations. The simultaneous discovery of bacteria and viruses in patients with acute exacerbation of COPD is responsible for the worsening lung function, prolonged hospital stay, and risk of recurrence of a similar event [5,6].

This study analyses the prevalence and pattern of viral and bacterial infections in patients presenting with acute exacerbation of COPD, correlates the type of infection with the severity of exacerbation among the patients, and finds out the long-term outcome of the severe follow-up cases after discharge in terms of readmission, clinical stability, or death.

Materials & Methods

The study was conducted from October 2018 to February 2022 among the patients admitted to critical care, Respiratory and General Medicine unit of Kalinga Institute of Medical Sciences, Bhubaneswar, in collaboration with Regional Medical Research Centre (ICMR), Bhubaneswar.

The sample size was calculated by using the formula: 

n = Z2 P(1−P)/d2

where n is the sample size; Z is the statistic corresponding to a 95% level of confidence, which is equal to 1.96; P is the expected prevalence (proportion of COPD patients with infectious etiology = 78.3% in a study conducted by Jahan et al.) [7]; d is the absolute precision (it has been taken as 6%). The sample size was found to be 179; adding a 10% non-response rate, the final sample size was 179 + 18 = 197.

Admitted cases underwent clinical assessment and other routine investigations. Empirical treatment was given as per standard treatment guidelines. The nasopharyngeal swab was taken and transported in a viral transport medium within 24 hours to the Regional Medical Research Centre (RMRC) for the detection of respiratory viruses. Samples were tested by real-time reverse transcription-polymerase chain reaction (RT-PCR). The test was done using recommended commercial kit (FTD, UK) following the manufacturer’s instructions on Applied Biosystems-7500 (ABI-7500) equipment (ABI, USA). After thorough rinsing of the oral cavity, respiratory secretions were sent in a sterile container to our institute laboratory for bacterial culture and sensitivity study by VITEK 2 compact instrument (bioMérieux, France).

Apart from the procedural guidelines, depending on the severity of the cases, patients were treated with microbe-targeted antibiotics, oxygen support, either parenteral or oral, nebulized corticosteroid, and bronchodilator and were classified as mild, moderate, and severe as per the GOLD guidelines. The severe cases underwent pulmonary physiotherapy (diaphragm strengthening, pursed-lip breathing, lower limb muscle training, and chest percussion) session one week after clinical stability.

The patients were contacted over telephonic/telemedicine services every three months (due to the COVID pandemic, physical follow-up was not done) to ensure that they were continuing to perform the exercises at home and consuming medications, and any clarifications sought were addressed. Outcome data were collected with respect to clinical stability, worsening of clinical symptoms requiring admission, or mortality at the end of one year of follow-up.

This is an observational follow-up study conducted in the pulmonary medicine department of the Kalinga Institute of Medical Sciences. Ethical clearance was obtained from Institutional Ethics Committee (vide letter no.: KIIT/KIMS/113). All patients (including those on ventilation) with acute exacerbation of COPD (based on acute onset of cough, increased sputum with or without purulence, and breathing difficulty) admitted to the pulmonary medicine department were included in the study. Patients with pulmonary tuberculosis (TB), bronchiectasis, bronchial asthma, pneumonia, and acute lung injury (based on history and evaluation) and patients unwilling to give consent were excluded from the study.

Statistical analysis

Descriptive statistics were done after the collection of data. Frequency distributions of categorical variables (occupation, gender, place of residence, smoking status, type of pathogens found, clinical features, comorbidities, and follow-up data) were calculated. For continuous data (age, total leukocyte count [TLC], and duration of hospital stays), mean and standard deviations were calculated. These were presented in tables using SPSS version 20.0 (IBM Corp., Armonk, NY) and Microsoft Excel 2007 (Microsoft Corporation, New Mexico, USA).

Type of infection, isolated organisms, and clinical outcomes after one year were identified. Chi-square and p-values were calculated to measure the associations between the type of infection and isolated organisms, type of infection, and readmission after one year.

Results

A total of 197 subjects were included in the study, out of which 138 (70.06%) were males and 59 (29.94%) were females. The maximum number of subjects (130 [65.9%]) were within the age group of 61-80 years. The total number of patients more than 80 years of age was 25 (12.69%). The mean age of the patients was 69.24 ± 11.08 years (Table 1).

Age group (years) Male Female Total
40-60 25 17 42
61-80 92 38 130
>80 21 4 25
Total 138 59 197

The total number of patients who had a smoking history was 126 (63.95%). Most of the study subjects were farmers (37.06%), and the least belonged to the category of laborer (2.54%). Out of the total subjects, only 83 (42.13%) patients were from rural areas (Table 2).

Variables Frequency Percentage (%)
Smoking history
Smoker 126 63.96
Non-smoker 71 36.04
Occupation
Teacher 16 8.12
Businessmen 21 10.66
Laborer 5 2.54
Farmer 73 37.06
Housewife 47 23.86
Unemployed 35 17.77
Area of residence
Urban 114 57.87
Rural 83 42.13

Out of 197 patients,102 (51.78%) had been isolated with bacteria or viruses, or both. Isolated viral infection was seen in 39 (19.79%) cases, while 46 (23.35%) had only bacterial exacerbations. In another 17 (8.62%) cases, both bacteria and viruses were detected. No etiology for exacerbation could be detected in 95 (48.2%) cases (Table 3).

Infection detected No. of cases Percentage (%)
Virus only 39 19.79
Bacteria only 46 23.35
Coinfection with both 17 8.62
No pathogen found 95 48.24
Total no. of patients 197 100

Out of 56 cases, in three cases of viral exacerbations, more than one virus (i.e., two) was detected, and in one case of viral exacerbation, more than one virus (i.e., three) was detected. A total of 62 viruses were isolated. Rhinovirus and Flu-A (H3N2) were isolated most frequently (30.35% and 25%, respectively) followed by respiratory syncytial virus (RSV) and parainfluenza virus 3 (PIV-3) (10.71% each; Table 4).

List of viruses No. of cases with viral infection (N = 56) % of patients with the isolated virus
Rhinovirus 17 30.35
Flu-A (H3N2) 14 25.0
RSV-B 6 10.71
Flu-B 4 7.14
PIV-3 6 10.71
Flu-A/PDM 09 4 7.14
HMPV 3 5.35
Adenovirus 2 3.57
RSV-A 2 3.57
COVID-19 4 7.14

A total of 63 bacteria were isolated in which gram-negative bacilli were most common, which include Acinetobacter baumanniiKlebsiella pneumoniae, and Pseudomonas aeruginosa. Among the gram positives, Staphylococcus aureus was the most common.

Rhinovirus was most commonly associated with bacterial coinfection in four cases (2.03%) followed by Flu-A and COVID-19. Acinetobacter baumannii was associated with a viral infection in most cases (five cases; 2.53%). This was followed by the detection of Pseudomonas aeruginosa and Klebsiella pneumoniae in two cases each (Table 5).

List of bacteria No. of cases with bacterial infection (N = 63) % of total bacteria isolated
Acinetobacter baumannii 14 22.22
Klebsiella pneumoniae 14 22.22
Pseudomonas aeruginosa 12 19.05
Staphylococcus aureus 5 7.94
Escherichia coli 8 12.70
Enterobacter cloacae complex 5 7.94
Serratia marcescens 2 3.17
Enterococcus faecium 1 1.59
Streptococcus pneumoniae 1 1.59
Staphylococcus haemolyticus 1 1.59
Sphingomonas paucimobilis 1 1.59

Breathlessness and cough were the most frequent complaints at the time of presentation. In cases with isolated viral exacerbation, 38 out of 39 cases (97.4%) had a shortness of breath, while 34 out of 39 (87.2%) cases had a cough. Fever was present in 14 out of 39 (32%) cases. However, sore throat was reported only in patients with isolated viral exacerbation, and chest pain was reported in patients with isolated bacterial exacerbations. Hypertension was the most common comorbidity reported in both bacterial and viral infections. Diabetes mellitus was mostly seen in patients who had a coinfection (Table 6).

Clinical feature Type of infection
Isolated viral Isolated bacterial Coinfection
Fever 14 19 6
Cough 34 36 13
Expectoration 9 10 4
Breathlessness 38 43 17
Chest pain 0 2 0
Sore throat 9 0 0
Altered sensorium 2 0 0
Comorbidities
Hypertension 11 16 4
Diabetes mellitus 5 5 6
Parkinson’s disease 0 2 0
Coronary artery disease 0 4 0
Cerebrovascular accident 1 2 0
Chronic kidney disease 1 1 0
Cushing syndrome 1 0 0
Chronic liver disease 1 0 0
Carcinoma larynx 0 1 0
Alzheimer’s disease 0 1 0
Congenital heart disease 0 0 1

Among the 102 patients with infective exacerbations, patients with viral exacerbation had relatively lower mean TLC, while patients with exacerbation due to coinfection had the highest mean TLC. However, the results were not significant (p = 0.641). Among the patients with infective exacerbations, those with viral exacerbation had the least mean duration of hospital stay (7.33 ± 4.8 days), while patients with bacterial exacerbation spent the highest number of days in the hospital (10.082 ± 5.89 days). The 17 patients with coinfection had a mean duration of hospitalization of 6.8 ± 5.03 days. The results were not statistically significant (p = 0.071). Ten (26%) patients with viral exacerbation, 24 (52%) with bacterial exacerbation, and nine (53%) patients with a coinfection required respiratory support and hence needed admission to ICU. Severity was most commonly noticed in coinfection cases (p = 0.020). Two deaths were reported in viral infections, four in bacterial exacerbation, and three in coinfections (Table 7).

Parameters Mean Value P-value
  Isolated viral infection (n = 39) Isolated bacterial infection (n = 46) Coinfection (n = 17)
Mean age (years ± SD) 68.36 ± 3.45 71.8 ± 11.73 73 ± 8.33 0.084NS
Total leukocyte count (cells/mm3) 11.139 ± 4.8 12.49 ± 5.435 12.66 ± 7.3 0.641NS
Mean duration of hospital stay (in days) 7.33 ± 4.8 10.052 ± 5.89 6.8 ± 5.03 0.071NS
Type of cases
Mild 12 (31%) 0 (0%) 0 (0%) 0.041S
Moderate 17 (43%) 22 (48%) 8 (47%) 0.062NS
Severe 10 (26%) 24 (52%) 9 (53%) 0.020S
No. of deaths among the severe cases 2 4 3 NA

The number of patients who had a severe disease was 43 (Table 7). Out of them, nine died. The rest 34 cases were advised pulmonary rehabilitation, oxygen therapy, inhaler-based medication as self-management home-based delivery, and were on telehealth monitoring. Five cases were lost to follow-up. In the rest 29 cases, information was documented after follow-up for one year that consisted of six viral infection, 17 bacterial infection, and six coinfection cases (Table 8).

Condition of the patients after one year of follow-up Viral infection (6 cases) Bacterial infections (17 cases) Coinfections (6 cases) P-value
Clinically stable 6 (100%) 16 (94%) 2 (33%) 0.034s
Exacerbation (admission) 0 1 (6%) 4 (67%)

All viral infection cases were clinically stable and did not require admission. Out of 17 bacterial infection cases, 16 (94%) were clinically stable and only one (6%) required hospital admission due to exacerbation. But in the six coinfection cases, two (33%) were clinically stable and the rest four (67%) cases required hospital admission, and the data was found to be statistically significant (p = 0.034). This shows most of the coinfection cases required rehospitalization during the period of follow-up (Table 8).

Discussion

Acute exacerbation of COPD results in deterioration of pulmonary function, morbidity, and death. In our study, the mean age of the patients was 69.24 ± 11.08 years with a majority of the patients belonging to the age group of 61-80 years (Table 1). In a recent study conducted at the All India Institute of Medical Sciences (AIIMS), Bhubaneswar, the mean age was 65.49 ± 10.40 years [7]. As per another Indian study by Mood et al., the mean age of patients was 66.8 ± 11.4 years and the maximum prevalence was observed in the age group 70-79 years [8]. In another study that involved both European and American subjects, the proportion of females was 36.7% among Europeans and 33.3% among Americans, which is in accordance with our findings [9]. A study by Hajare et al. reported a male-to-female ratio of 2.3:1 [10]. The preponderance of males being affected can be attributed to the fact that males are more involved in outdoor activities and hence are more exposed to environmental pollutants [8]. Smoking is a risk factor for COPD and also its exacerbation as it decreases mucociliary clearance, which is amply proved in our study where smoking as a risk factor was noticed among 64% of patients [11]. In our study, the two main occupations that had increased the prevalence of COPD were farmers and housewives (Table 2). In a study published in 2016, occupations that were at COPD risk were seafarers, coalmine operatives, and cleaners [12]. In a study in Bangladesh, occupational exposures in farmers, hazardous exposures in tanners, and cotton dust exposures in garments were among the most prominent risk factors for the development of COPD [13]. In our study, the urban population comprised the majority (57.8%, Table 2), which correlates well with a study done in India where the prevalence of COPD was more in the urban areas. But there has been a significant increase in the prevalence in rural areas where it was reported to be 8.8% in a study done in India, whereas in our study, the prevalence is around 22% [14]. The disparity in the urban-rural divide is reversed in the United States, where the prevalence of COPD in rural communities is nearly double that in urban areas [15].

The complex interactions between environment, host, and microbes are responsible for exacerbations in COPD and increased morbidity and mortality [16]. As per studies, the major cause of acute exacerbations is infections [7]. In our study, infection was detected in 51.7% of cases (Table 3). In an Indian study, around 78.3% of cases had a respiratory infection [7]. Our study illustrates that only bacterial infection was found in 23.35% of cases; only viral etiology was found in 19.79% of cases, and bacterial and viral coinfection was found in 8.62% of cases. Other studies have reported bacterial infection in around 42%-49% of cases, viral infections in around 20%-64% of cases, and bacterial-viral coinfection in 27% of cases [7,17,18]. There has been an increased report of respiratory viruses as a causative agent in the acute exacerbation of COPD. With the application of molecular techniques in patients’ samples, viruses have been implicated in around 47%-66% of cases [11]. A total of 56 viruses were isolated (Tables 3, 4). The most common viruses isolated were rhinovirus, followed by Flu-A and RSV-B. Human rhinovirus (HRV) has been reported as a common viral isolate in various studies [18]. The study by Koul et al. also reported rhinovirus and influenza virus as the most common virus causing acute exacerbation of COPD [19]. The high rate of isolation of influenza virus may be attributed to the transmission of the influenza virus in the community and the need to have immunization [20]. In our study, more than one virus was isolated in three cases. Similar results have been found in a recent study in India [7]. The most common bacterial isolates in our study are Acinetobacter baumannii, Klebsiella pneumoniae, and Pseudomonas aeruginosa making up around 21.9% (for both Acinetobacter and Klebsiella) and 18.8%, respectively. Among the gram-positive bacteria, Staphylococcus aureus (7.8%), Enterococcus faecium (1.6%), and Streptococcus pneumoniae (1.6%) were the most common isolates. In the study by Jahan et al., the most common bacteria isolated were Pseudomonas aeruginosa (28%), followed by Acinetobacter baumannii and Klebsiella pneumoniae in seven cases each (21%) [7]. In another study, the most common bacterial isolates were P. aeruginosa (30.7%) followed by K. pneumoniae (20.3%) and S. pneumoniae (8.6%) [8].

It is to be noted that most of the studies implicate Pseudomonas aeruginosa as the most common bacteria causing exacerbation, whereas Acinetobacter baumannii and Klebsiella pneumoniae are the most common bacteria causing exacerbations as per (Table 5) of our study [21]. The predominance of Acinetobacter spp. in our study is a novel finding, and further studies are needed to know if this is the emerging trend in acute exacerbation of COPD as MDR (multidrug-resistant). Acinetobacter baumannii is implicated in the etiology of various other infections [22]. Jahan et al. reported coinfection with virus and bacteria in 24.9% of cases of acute exacerbations of COPD [7]. In our study, coinfection was detected in 9.63% of cases (Table 3). However, this may not represent a natural course as many patients are chronically infected with multiple pathogenic bacteria before a viral pathogen is detected. Conversely, viruses have been shown to be frequently followed by secondary bacterial infection. Most of the coinfections were seen to be associated with rhinovirus and influenza A virus, whereas it was mostly associated with both influenza A and influenza B in another study by Jahan et al. [7]. In another study, the viruses implicated alone or as coinfections are picornaviruses (especially rhinovirus), influenza virus, and respiratory syncytial virus [23]. Comorbidities were associated with eight cases of viral exacerbation with hypertension being the most common (Table 6). Similar findings were also reported by Koul et al. where hypertension was seen in 60.52% of cases followed by heart ailments (14.16%) [19]. No significant correlation was observed between the various subgroups. Breathlessness and cough were the most common clinical presentation in cases of exacerbation in our study. Sore throat, however, was reported only in viral exacerbation and not in bacterial or coinfection (Table 6). The outcome of viral exacerbation has improved over time, owing to an increase in adult vaccination and early treatment. Among the etiological agents, in our study, we noticed poor outcomes among the coinfection group probably as a consequence of systemic inflammation (Table 7). As per a study in Japan, gram-negative bacilli were significantly associated with prolonged hospitalization [24].

The severe category of patients who were discharged was put on telemedicine advice on pulmonary physiotherapy, medications, and home oxygen. Among them, the coinfection group had exacerbation that needed admission, and the rest of the cases were clinically stable (Table 8). There are not many studies that correlate the long-term outcome of acute exacerbation of COPD with infective causes. As per a review by Wang et al., it is observed that in cases where there is coinfection with bacteria and virus, the lung function impairment is greater and the duration of hospitalization is also longer [25]. In another study published in Lung India, where the outcomes were followed up for readmission for two years, 12% mortality was observed; readmission was seen in 54% of cases, and two or more readmissions were seen in 45% of cases [26].

Thus, a proportion of patients appear to be more susceptible to exacerbation. Hence, prevention and mitigation should be the key goals. The application of technological advancement in communication during the COVID pandemic enabled us to overcome the challenge through tailored prescription and telemedicine intervention.

Conclusions

The clinical course of COPD is punctuated by exacerbation. These events are associated with accelerated loss of lung function, poor quality of life, increased health care costs, and mortality. Infection is the most important cause of exacerbation. Klebsiella pneumoniae and Acinetobacter baumannii among the bacterial isolates and rhino and influenza A viruses among the viral isolates were predominantly detected. During the telehealth follow-up, it was observed that those patients who had co-infections were more prone to readmission, whereas those who had isolated bacterial or viral etiology had better clinical stability. Pulmonary physiotherapy and appropriate medical measures for the mitigation of exacerbation can prevent further decline of disease progression.



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Asthma is a lung condition in which the airways become inflamed and narrowed. This narrowing restricts the amount of air that can move through the bronchioles and usually causes distinct breathing sounds such as wheezing and coughing.

In silent asthma, no wheezing or coughing is present. This may be a variation in asthma symptoms, or it could be a phenomenon that healthcare providers sometimes refer to as the "silent chest." Silent chest can be associated with severe forms of asthma, including status asthmaticus and fatal asthma.

This article discusses the causes of silent asthma as well as symptoms, diagnosis, treatment, and prevention.

Karl Tapales / Getty Images


Silent Asthma Symptoms

Silent asthma symptoms are similar to those of regular asthma, with the absence of coughing or wheezing. Symptoms may include:

  • Distress, anxiety, or restlessness
  • Fatigue
  • Chest tightness
  • Feeling short of breath
  • Difficulty speaking

Severe symptoms that require immediate medical attention may include:

  • Breathing retractions that look like an area of sinking or sucking in that occurs when breathing muscles are working hard (retractions may be most noticeable between the ribs or at the base of the neck)
  • Rapid breathing
  • Inability to talk due to difficulty breathing
  • Cyanosis (bluish color around the lips or beds of the fingernails, which indicates poor oxygenation)
  • Dizziness or passing out

Causes

A specific cause of asthma cannot always be identified. However, there are some known risk factors for the development of asthma:

  • Genetics
  • Allergies
  • Environmental factors, such as exposure to pollution
  • Respiratory infections
  • Obesity

It's worth noting that the term "silent asthma" is not well-defined or researched. If you have been told that you have silent asthma by a healthcare provider, it could simply mean that you are have mild or moderate symptoms of asthma without wheezing or coughing.

However, at some point, almost everyone with asthma will experience wheezing and coughing, even if you don't experience the more audible symptoms all the time.

One reason you may not have wheezing or coughing is that your airways have not tightened so much as to restrict air movement through your bronchioles, or at least not enough to produce these characteristic breathing noises.

It's also possible that you are wheezing, but it is so faint that it's difficult to hear. Not everyone with asthma experiences the same symptoms, and your symptoms may vary depending on the day and circumstance.

Status Asthmaticus and Silent Chest

Status asthmaticus is a severe form of asthma that doesn't respond well to typical treatments. An individual with status asthmaticus can experience such a severe asthma attack that it leads to silent chest. Silent chest is the absence of wheezing and coughing due to fatigue and inability to move any air through severely constricted bronchioles. Silent chest usually precedes respiratory failure and is a life-threatening medical emergency.

Diagnosis

If your healthcare provider suspects asthma based on your symptoms, physical examination, and medical history, they might order one or more of the following tests to confirm the diagnosis:

Treatment

There are several differ treatment options for asthma, including medication, procedures, and avoiding triggers.

Triggers

Triggers are anything that brings on asthma symptoms. Identifying and avoiding asthma triggers can be an important part of your treatment plan.

Potential asthma triggers include:

  • Allergens (i.e., mold, pollen, pet dander)
  • Air pollution
  • Chemicals or toxins (i.e., tobacco smoke, cleaning supplies, paint fumes)
  • Exercise

Medications

Long-acting or maintenance medications for asthma work to prevent asthma attacks. These include:

Short-acting or rescue medications for asthma relieve the symptoms of an acute asthma attack. They include:

Bronchothermoplasty

Bronchothermoplasty is a procedure used to treat severe asthma that cannot be controlled with other treatments. It involves using a bronchoscope to apply heat to the muscles of the bronchioles, which thins and weakens the muscles, making it more difficult for them to constrict during an asthma attack.

Asthma Action Plan

Another name for your treatment regimen is an asthma action plan. An asthma action plan is a plan you develop with your healthcare provider that outlines how to prevent and treat asthma symptoms. It should clearly define what medications you should use and when, as well as when you need to seek professional medical help, including when to call 911.

Preventing Asthma Attacks

The best way to prevent asthma attacks is to stick to your asthma action plan. In particular, make sure to use your long-acting asthma medications on time and as prescribed, and identify and avoid triggers.

Summary

While wheezing and coughing are classic symptoms of asthma, it is possible to have asthma without experiencing these symptoms. This is known as silent asthma. This form of asthma can include a mild to moderate variation of symptoms. However, if it occurs after a prolonged asthma attack or is accompanied by serious symptoms, such as cyanosis or loss of consciousness, it could be a life-threatening condition called silent chest.

If you suspect silent chest, call 911 or go to your nearest emergency room.

A Word From Verywell

Silent asthma can be a particularly frightening condition because the lack of obvious symptoms makes it more difficult to diagnose. While there is no cure for asthma, symptoms can be managed once a diagnosis is made. The best way to manage the condition is to create an asthma action plan with a qualified healthcare provider and stick to it.

Frequently Asked Questions

  • Can you have asthma without knowing?

    Yes, it is possible to have asthma without knowing it, especially if your symptoms are mild or atypical. If you suspect asthma or any kind of respiratory condition, you should consult a healthcare provider for a proper diagnosis.

  • What can be mistaken for asthma?

    The symptoms of asthma can mimic many other health conditions including COPD, GERD, respiratory infections, sarcoidosis, pulmonary hypertension, pulmonary embolism, bronchiectasis, eosinophilic bronchitis, and allergic rhinitis to name a few.

  • What does silent asthma feel like?

    Silent asthma may feel like a tightening of your chest, shortness of breath, and difficulty speaking. You may also feel anxious and unable to hold still.

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1Department of Respiratory, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, People’s Republic of China; 2Department of Respiratory Medicine, Shengli Oilfield Central Hospital, Dongying, People’s Republic of China; 3Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, People’s Republic of China

Correspondence: Liang Dong, Department of Respiratory, Shandong Provincial Qianfoshan Hospital, Shandong University, The First Affiliated Hospital of Shandong First Medical University, Shandong Institute of Respiratory Diseases, Jinan, 250014, People’s Republic of China, Tel +86-13505401207, Email [email protected]

Background: Interleukin (IL)-36α, IL-36β, and IL-36γ belong to the IL-36 family and play an important role in the pathogenesis of many diseases. Chronic obstructive pulmonary disease (COPD) may be correlated with IL-36; however, the specific role of IL-36 in COPD is unclear. In this study, we aimed to clarify whether IL-36 could be an indicator for determining COPD severity and the specific nature of the pro-inflammatory effects of IL-36 in COPD.
Methods: A total of 70 patients with COPD and 20 control subjects were included in this study. We collected peripheral blood samples from both the groups, analyzed the blood cell fractions by routine blood examination, and measured the serum levels of IL-36α, IL-36β, and IL-36γ by performing polymerase chain reaction and enzyme-linked immunosorbent assay. In addition, the correlation between the number of neutrophils and eosinophils and the level of IL-36 was also analyzed.
Results: We found that level of IL-36 in patients with COPD was positively correlated with the number of neutrophils but not with eosinophils, whereas the correlation was not found in the control group. Moreover, the level of IL-36 was negatively correlated with the level of lung function of patients with COPD, and the levels of IL-36α, IL-36β, and IL-36γ increased with advancing disease severity.
Conclusion: In COPD, the pro-inflammatory effect of IL-36 is closely related to neutrophils, and hence, IL-36 might be considered a novel biomarker for determining COPD severity.

Keywords: chronic obstructive pulmonary disease, IL-36, neutrophils, inflammation

Introduction

Chronic obstructive pulmonary disease (COPD) is a heterogeneous, inflammatory-airway disease. As the disease is characterized by high morbidity and mortality, approximately 200 million people worldwide are affected and more than 3 million deaths occur each year.1,2 Unfortunately, epidemiological data could not adequately reflect the widespread impact and disease burden caused by COPD because, in many lagging regions, the diagnosis rate of COPD is much lower than the true picture.3 The most critical feature of COPD is irreversible airflow limitation, and its typical pathogenesis includes airway remodeling, emphysematous lung parenchymal destruction, and airway inflammatory response.4 Airway inflammation in COPD involves various cells such as neutrophils, lymphocytes, monocytes, and dendritic cells.5,6 Among these cells, the association of neutrophils with COPD has been widely studied; neutrophil levels are significantly higher in sputum and bronchoalveolar lavage fluid of patients with COPD than those in healthy individuals.7–9 In addition, the number and distribution range of neutrophils were significantly increased in animal models of COPD.10,11 As neutrophils are closely associated with COPD, neutrophilic inflammation is undoubtedly an important part of the pathogenesis of COPD. Therefore, investigating the effect of related cytokines on neutrophilic inflammation will certainly enhance the understanding of COPD pathogenesis.

As a member of the interleukin (IL)-1 family, IL-36 has two classes of four isomers, namely IL-36α, IL-36β, IL-36γ, and IL-36Ra.12 IL-36α, IL-36β, and IL-36γ belong to the group of agonists that promote many diseases such as psoriasis, arthritis, and allergic rhinitis.13–15 On the other hand, IL-36Ra belongs to the group that mainly plays a role in counteracting the effects of IL-36.16 IL-36 is widely distributed in several vital organs such as the heart, brain, and kidney.17–19 Different IL-36 isoforms play different roles in diseases, either synergistically or counteracting each other.20 For example, IL-36α could trigger the activation of the IL-23/IL-17A signaling axis and thus induce an inflammatory response leading to psoriasis,21 whereas IL-36Ra could suppress skin inflammation and provide protection.22 IL-36β could increase the expression of IL-6 and CXCL8 in human lung fibroblasts and bronchial epithelial cells,23 and IL-36γ could promote the recruitment of Th17 cells and the activation of fibroblasts.24 As a typical chronic airway disease, the association of COPD with IL-36 has been demonstrated in several studies. For example, some studies reported that IL-36α and IL-36γ levels in sputum were significantly increased in patients with COPD,25 whereas the level of IL-36 decreased in patients with COPD with eosinophilic phenotype.26 Combined with the importance of neutrophils in COPD pathogenesis, we inferred that IL-36 is correlated with neutrophils in COPD pathogenesis. To further elucidate the mechanism underlying COPD pathogenesis, the correlation between IL-36 and neutrophils should be investigated.

Hence, we hypothesized that IL-36 could promote COPD pathogenesis by promoting a neutrophilic inflammatory response, and the level of IL-36 is closely related to the severity of COPD. To verify this hypothesis, we performed a polymerase chain reaction and enzyme-linked immunosorbent assay. In addition, the correlation between the number of neutrophils and eosinophils and the level of IL-36 was also analyzed. This study is expected to bring a new perspective to the diagnosis and treatment of COPD.

Materials and Methods

Subjects

Between March and September 2021, we enrolled patients with COPD (n = 70) and control subjects (n = 20) from the Shandong Provincial Qianfoshan Hospital. The characteristics of patients with COPD and control subjects are shown in Table 1. The diagnosis of COPD was in accordance with the Global Initiative for Chronic Obstructive Lung Disease (GOLD, 2021 edition). According to the GOLD criteria for the severity of disease, we divided the patients with COPD into 4 subgroups: GOLD 1 (n = 6), GOLD 2 (n = 21), GOLD 3 (n = 33), and GOLD 4 (n = 10). For the enrolled patients with COPD, all the following conditions were excluded: (i) Pulmonary disease other than COPD such as lung cancer, nodular disease, active tuberculosis, pulmonary fibrosis, and cystic fibrosis; (ii) Previous acute exacerbation of COPD within 4 weeks; (iii) Inflammatory diseases other than COPD such as rheumatoid arthritis, systemic lupus erythematosus, and inflammatory bowel disease; (iv) Lung surgery or recently diagnosed malignant tumor; (v) Unable to walk; (vi) Received blood transfusion within 4 weeks; (vii) Receiving systemic hormone therapy; (viii) Participating in any double-blind drug clinical trial. The subjects in the control group showed normal lung function and had no airflow limitation. For the enrolled control subjects, the following conditions were excluded: asthma, bronchiectasis, pulmonary abscess, interstitial lung disease, tuberculosis, central lung mass, systematic disease such as congestive heart failure, autoimmune disease, and infection. All patients voluntarily entered the study and signed the written informed consent. The study was conducted in accordance with the declaration of Helsinki. The study was approved by the Ethics Committee of the Shandong Provincial Qianfoshan Hospital.

Table 1 Characteristics of COPD Patients and Control Subjects

Peripheral Venous Blood Processing

We collected peripheral blood samples from all the enrolled individuals. The amount of blood samples was generally 5–10 mL due to the different cooperation of each person. One portion of the blood sample was centrifuged for 10 min at 1500 g at 4°C for basal experiments, and the remaining was used for routine blood examination. After separating the upper serum layer, we performed density-gradient centrifugation to collect the peripheral blood mononuclear cells (PBMCs).

Reverse Transcription and Quantitative-Polymerase Chain Reaction (qPCR)

All steps for the qPCR were performed according to the instructions provided with the kit. Total RNA from PBMCs was extracted using the RNAfast200 kit (Fastagen, Shanghai, China). The Evo M-MLV RT kit was used to synthesize cDNA (AG, Hunan, China). The SYBR® Green Premix Pro Taq HS qPCR kit (AG, Hunan, China) was used to quantify mRNA. GAPDH served as the internal reference for this experiment. The 2−ΔΔCT method was used to calculate the experimental results. The primer sequences used in this study are listed in Table 2.

Table 2 Primers for qRT-PCR

Enzyme-Linked Immunosorbent Assay (ELISA)

Blood samples were obtained from every participant, and serum was obtained and stored at −80°C until use. The serum levels of IL-36α (Solarbio, Beijing, China), IL-36β (Solarbio, Beijing, China), and IL-36γ (Abcam, Cambridge, UK) were measured using the corresponding ELISA kits following the manufacturers’ protocols.

Statistical Analyses

The patient characteristics were expressed as the mean ± standard deviation (SD) or the median (IQR). Count data were analyzed using the Chi-square test, and the measurement data were based on the distribution using the unpaired t-test for normal distribution and the Mann–Whitney test for skewed distribution. Correlations were calculated using Spearman’s rank correlation analyses. All statistical analyses were performed using the SPSS 25 (Abbott Laboratories, USA). The differences were considered to be statistically significant at the two-sided p-value of <0.05.

Results

Patient Characteristics

No significant differences were found between the COPD and control groups in terms of gender, age, BMI, and smoking status. Lung function was significantly worse in the COPD group than in the control group, which is not surprising (Table 1).

Peripheral Venous Blood Cell Counts

To determine the association of neutrophils and eosinophils with COPD, we compared the differences between the COPD and control groups in terms of neutrophil count and eosinophil count obtained by routine blood examination. The results showed that the COPD group had a higher number and proportion of neutrophils but lower eosinophil content compared with the control group. This result indicated the possible association of neutrophils and eosinophils with COPD (Table 1).

IL-36 Could Promote COPD Development and is an Indicator for Determining COPD Severity

To clarify the association between IL-36 and COPD, we measured the levels of IL-36α, IL-36β, and IL-36γ in the serum of patients and control subjects by performing ELISA. The results showed that the levels of IL-36α, IL-36β, and IL-36γ were higher in patients than in control subjects, and the levels of IL-36α, IL-36β, and IL-36γ increased with the progression of the disease (Figure 1).

Figure 1 IL-36 was highly expressed in patients with COPD and was related to the severity of COPD. The levels of the IL-36α (A), IL-36β (B), and IL-36γ (C) in the serum of patients with COPD were measured using the ELISA kit. The number of samples in each group was as follows, GOLD 1 (n = 6), GOLD 2 (n = 20), GOLD 3 (n = 20), GOLD 4 (n=9), Control (n = 15). Data were pooled from at least 3 independent experiments and are presented as the mean ±SD. *p < 0.05, **p < 0.01.

To further confirm the association between IL-36 and COPD, PBMCs from both groups were analyzed by performing PCR. The PCR results are consistent with the ELISA results. The results of PCR showed that the mRNA level of IL-36 increased with the GOLD grading. The mRNA levels of IL-36 were statistically different in COPD patients with different GOLD grading. Thus, IL-36 could promote the development of COPD and the level of IL-36 might be considered an indicator for determining COPD severity (Figure 2).

Figure 2 IL-36 was highly expressed in patients with COPD and was related to the severity of COPD. The mRNA levels and significant differences in IL-36α (A), IL-36β (B), and IL-36γ (C) in PBMCs of patients with COPD were determined by PCR. The number of samples in each group was as follows, GOLD 1 (n = 6), GOLD 2 (n = 20), GOLD 3 (n = 20), GOLD 4 (n=9), Control (n = 15). Data were pooled from at least 3 independent experiments and are presented as the mean ±SD. *p < 0.05, **p < 0.01.

COPD, IL-36 is Closely Associated with Neutrophils

As IL-36 is a pro-inflammatory factor, the association between IL-36 and COPD is most likely based on neutrophils or eosinophils. To elucidate the mechanism underlying the pro-inflammatory effect of IL-36 in COPD, we analyzed the correlation between the levels of IL-36α, IL-36β, and IL-36γ and the number of neutrophils and eosinophils. The results showed that the levels of IL-36α (r = 0.5578, p < 0.0001), IL-36β (r = 0.4511, p < 0.01), and IL-36γ (r = 0.6908, p < 0.0001) in serum were positively correlated with the number of neutrophils, but not with the number of eosinophils in patients with COPD (Figure 3). In addition, IL-36 levels in patients with COPD were negatively correlated with their lung function levels. For control subjects, no significant association was found between IL-36 level and the number of neutrophils or eosinophils (Figure 4). To conclude, the pro-inflammatory factors IL-36α, IL-36β, and IL-36γ could promote neutrophilic inflammatory responses in COPD and hence might be considered novel, potential targets for determining COPD severity.

Figure 3 In COPD, IL-36 was closely related to neutrophils. (A–C) Correlation analysis of IL-36 and neutrophils in the COPD group. (D–F) Correlation analysis of IL-36 and eosinophils in the COPD group. (G–I) Correlation analysis of IL-36 and the lung functions in the COPD group.

Figure 4 For control subjects, the IL-36 levels were not related to the number of inflammatory cells. (A–C) Correlation analysis of IL-36 and neutrophils in the control group. (D–F) Correlation analysis of IL-36 and eosinophils in the control group.

Discussion

COPD is a chronic airway disease with high rates of morbidity, disability, and mortality. Despite its low diagnosis rate in economically disadvantaged regions, an epidemiological survey conducted in 2015 showed that COPD ranked third in age-standardized mortality rates for men and women worldwide, after ischemic heart disease and cerebrovascular disease.27 To reduce the heavy disease burden associated with COPD, studies on the pathogenesis of COPD are required. Several important factors have been identified that trigger COPD, such as smoking, air pollution, and the presence of susceptibility genes.28,29 However, the identification of these factors has not facilitated substantial progress in COPD treatment because each factor has its limitations, such as the presence of several nonsmokers among patients with COPD and the difficulty of implementing effective interventions at the genetic level. Hence, COPD is difficult to treat, and even though some studies have shown that inhaling glucocorticoids combined with dual bronchodilators can reduce the incidence of acute exacerbations in COPD, the effect is less pronounced than that in the treatment of other diseases such as asthma.30,31 To improve the efficiency of COPD diagnosis and treatment, exploring its pathogenesis and identifying new targets are crucial.

As a member of the IL-1 superfamily, IL-36 contains two classes of mutually antagonistic factors.12 IL-36Ra belongs to one class, which plays an anti-inflammatory protective role in many tissues such as epithelial tissues.32,33 IL-36α, IL-36β, and IL-36γ belong to another class, and many studies have demonstrated the pro-inflammatory and pro-fibrotic functions of this class of molecules. For example, IL-36α activates the IL-23/IL-17A signaling pathway in psoriasis;21 IL-36γ promotes eosinophil activation and migration in allergic rhinitis;34 IL-36β plays a pro-inflammatory role in arthritis.35 A study has shown that IL-36 agonist molecules (IL-36α, IL-36β, and IL-36γ) exert their effects mainly via myeloid differentiation factor 88, mitogen-activated protein kinase, and nuclear factor kappa-B signaling pathways.36 The association of COPD with IL-36 agonist molecules has been demonstrated in a few studies;37,38 however, it is unclear. In this study, we attempted to explore the pro-inflammatory role of IL-36 agonist molecules in COPD and to determine whether an association exists between IL-36 levels and COPD severity.

To verify the association between IL-36 and COPD, the COPD and control groups with no difference in the baseline status (age, sex, BMI, and smoking status) were included in the study. We then collected serum samples from both the groups and measured IL-36α, IL-36β, and IL-36γ levels by performing ELISA. The results showed that the levels of IL-36 agonist molecules were significantly higher in the COPD group than in the control group, and the levels of IL-36 increased with the aggravation of the disease. To further confirm this association, PBMCs were extracted from peripheral blood obtained from both the groups, and PCR was performed. The PCR results and the ELISA results are consistent. These results suggested that the levels of IL-36 agonist molecules are correlated with COPD pathogenesis and hence might be considered as indicators for determining COPD severity.

Neutrophils and eosinophils are two critical types of cells in the airway inflammatory response.39 As IL-36 agonist molecules can exert their pro-inflammatory effects in COPD, we determined which cells among the two types are responsible for these pro-inflammatory effects. We analyzed the correlation between IL-36 levels and peripheral blood neutrophil and eosinophil counts in the two groups. The results demonstrated that levels of IL-36α, IL-36β, and IL-36γ correlated with the number of neutrophils but not with eosinophils in patients with COPD. The levels of IL-36 in control subjects were not correlated with the number of either cell type. Thus, IL-36 could induce COPD mainly by promoting neutrophilic inflammation.

Conclusion

Although the study is not complex and has some limitations such as the relatively small number of participants, the use of only serological experiments, and the absence of a wider variety of samples, the originality and value of this study are pronounced. This study is the first to report the possible association between il-36 and COPD at the circulating level. This study not only demonstrated that IL-36 induces COPD by promoting neutrophilic inflammation but also indicated the possibility of IL-36 as a novel predictor of COPD severity. Although this study focuses more on clinical findings than on the molecular mechanisms underlying this phenomenon, further research is expected to bring new breakthroughs in the treatment of COPD.

Data Sharing Statement

Experimental data related to this study can be obtained from the corresponding author upon reasonable request.

Ethical Approval

All studies involving human participants were conducted in accordance with the standards specified by the Ethics Committee of Shandong Provincial Qianfoshan Hospital. This study is in line with the Declaration of Helsinki.

Funding

This work was funded by the National Natural Science Foundation of China (Grant No. 81770029).

Disclosure

The authors declare no conflicts of interest in this work.

References

1. Rabe KF, Watz H. Chronic obstructive pulmonary disease. Lancet. 2017;389(10082):1931–1940. doi:10.1016/S0140-6736(17)31222-9

2. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388(10053):1545–1602. doi:10.1016/S0140-6736(16)31678-6

3. Lamprecht B, Soriano JB, Studnicka M, et al. Determinants of underdiagnosis of COPD in national and international surveys. Chest. 2015;148(4):971–985. doi:10.1378/chest.14-2535

4. O’Donnell DE. Hyperinflation, dyspnea, and exercise intolerance in chronic obstructive pulmonary disease. Proc Am Thorac Soc. 2006;3(2):180–184. doi:10.1513/pats.200508-093DO

5. Barnes PJ, Shapiro SD, Pauwels RA. Chronic obstructive pulmonary disease: molecular and cellular mechanisms. Eur Respir J. 2003;22(4):672–688. doi:10.1183/09031936.03.00040703

6. Brusselle GG, Joos GF, Bracke KR. New insights into the immunology of chronic obstructive pulmonary disease. Lancet. 2011;378(9795):1015–1026. doi:10.1016/S0140-6736(11)60988-4

7. Ravi AK, Khurana S, Lemon J, et al. Increased levels of soluble interleukin-6 receptor and CCL3 in COPD sputum. Respir Res. 2014;15(1):103. doi:10.1186/s12931-014-0103-4

8. Martin TR, Raghu G, Maunder RJ, Springmeyer SC. The effects of chronic bronchitis and chronic air-flow obstruction on lung cell populations recovered by bronchoalveolar lavage. Am Rev Respir Dis. 1985;132(2):254–260. doi:10.1164/arrd.1985.132.2.254

9. Hunninghake GW, Gadek JE, Kawanami O, Ferrans VJ, Crystal RG. Inflammatory and immune processes in the human lung in health and disease: evaluation by bronchoalveolar lavage. Am J Pathol. 1979;97(1):149–206.

10. Dhami R, Gilks B, Xie C, Zay K, Wright JL, Churg A. Acute cigarette smoke-induced connective tissue breakdown is mediated by neutrophils and prevented by alpha1-antitrypsin. Am J Respir Cell Mol Biol. 2000;22(2):244–252. doi:10.1165/ajrcmb.22.2.3809

11. Lams BE, Sousa AR, Rees PJ, Lee TH. Immunopathology of the small-airway submucosa in smokers with and without chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1998;158(5 Pt 1):1518–1523. doi:10.1164/ajrccm.158.5.9802121

12. Yuan ZC, Xu WD, Liu XY, Liu XY, Huang AF, Su LC. Biology of IL-36 signaling and its role in systemic inflammatory diseases. Front Immunol. 2019;10:2532. doi:10.3389/fimmu.2019.02532

13. Ainscough JS, Macleod T, McGonagle D, et al. Cathepsin S is the major activator of the psoriasis-associated proinflammatory cytokine IL-36γ. Proc Natl Acad Sci U S A. 2017;114(13):E2748–E2757. doi:10.1073/pnas.1620954114

14. Frey S, Derer A, Messbacher ME, et al. The novel cytokine interleukin-36α is expressed in psoriatic and rheumatoid arthritis synovium. Ann Rheum Dis. 2013;72(9):1569–1574. doi:10.1136/annrheumdis-2012-202264

15. Qin X, Zhang T, Wang C, Li H, Liu M, Sun Y. IL-36α contributes to enhanced T helper 17 type responses in allergic rhinitis. Cytokine. 2020;128:154992. doi:10.1016/j.cyto.2020.154992

16. Yi G, Ybe JA, Saha SS, et al. Structural and functional attributes of the Interleukin-36 receptor. J Biol Chem. 2016;291(32):16597–16609. doi:10.1074/jbc.M116.723064

17. Queen D, Ediriweera C, Liu L. Function and regulation of IL-36 signaling in inflammatory diseases and cancer development. Front Cell Dev Biol. 2019;7:317. doi:10.3389/fcell.2019.00317

18. Berglöf E, Andre R, Renshaw BR, et al. IL-1Rrp2 expression and IL-1F9 (IL-1H1) actions in brain cells. J Neuroimmunol. 2003;139(1–2):36–43. doi:10.1016/S0165-5728(03)00130-9

19. Nishikawa H, Taniguchi Y, Matsumoto T, et al. Knockout of the interleukin-36 receptor protects against renal ischemia-reperfusion injury by reduction of proinflammatory cytokines. Kidney Int. 2018;93(3):599–614. doi:10.1016/j.kint.2017.09.017

20. Murrieta-Coxca JM, Rodríguez-Martínez S, Cancino-Diaz ME, Markert UR, Favaro RR, Morales-Prieto DM. IL-36 cytokines: regulators of inflammatory responses and their emerging role in immunology of reproduction. Int J Mol Sci. 2019;20(7):1649. doi:10.3390/ijms20071649

21. Milora KA, Fu H, Dubaz O, Jensen LE. Unprocessed Interleukin-36α regulates psoriasis-like skin inflammation in cooperation with Interleukin-1. J Invest Dermatol. 2015;135(12):2992–3000. doi:10.1038/jid.2015.289

22. Blumberg H, Dinh H, Trueblood ES, et al. Opposing activities of two novel members of the IL-1 ligand family regulate skin inflammation. J Exp Med. 2007;204(11):2603–2614. doi:10.1084/jem.20070157

23. Zhang J, Yin Y, Lin X, et al. IL-36 induces cytokine IL-6 and chemokine CXCL8 expression in human lung tissue cells: implications for pulmonary inflammatory responses. Cytokine. 2017;99:114–123. doi:10.1016/j.cyto.2017.08.022

24. Ramadas RA, Ewart SL, Medoff BD, LeVine AM. Interleukin-1 family member 9 stimulates chemokine production and neutrophil influx in mouse lungs. Am J Respir Cell Mol Biol. 2011;44(2):134–145. doi:10.1165/rcmb.2009-0315OC

25. Li W, Meng X, Hao Y, Chen M, Jia Y, Gao P. Elevated sputum IL-36 levels are associated with neutrophil-related inflammation in COPD patients. Clin Respir J. 2021;15(6):648–656. doi:10.1111/crj.13338

26. Moermans C, Damas K, Guiot J, et al. Sputum IL-25, IL-33 and TSLP, IL-23 and IL-36 in airway obstructive diseases. Reduced levels of IL-36 in eosinophilic phenotype. Cytokine. 2021;140:155421. doi:10.1016/j.cyto.2021.155421

27. GBD 2015 Mortality and Causes of Death Collaborators. Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388(10053):1459–1544. doi:10.1016/S0140-6736(16)31012-1

28. Eisner MD, Iribarren C, Yelin EH, et al. The impact of SHS exposure on health status and exacerbations among patients with COPD. Int J Chron Obstruct Pulmon Dis. 2009;4:169–176. doi:10.2147/COPD.S4681

29. Peacock JL, Anderson HR, Bremner SA, et al. Outdoor air pollution and respiratory health in patients with COPD. Thorax. 2011;66(7):591–596. doi:10.1136/thx.2010.155358

30. Wedzicha JA, Banerji D, Chapman KR, et al. Indacaterol-Glycopyrronium versus Salmeterol-Fluticasone for COPD. N Engl J Med. 2016;374(23):2222–2234. doi:10.1056/NEJMoa1516385

31. Pascoe SJ, Lipson DA, Locantore N, et al. A Phase III randomised controlled trial of single-dose triple therapy in COPD: the IMPACT protocol. Eur Respir J. 2016;48(2):320–330. doi:10.1183/13993003.02165-2015

32. Towne JE, Renshaw BR, Douangpanya J, et al. Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36α, IL-36β, and IL-36γ) or antagonist (IL-36Ra) activity. J Biol Chem. 2011;286(49):42594–42602. doi:10.1074/jbc.M111.267922

33. Günther S, Sundberg EJ. Molecular determinants of agonist and antagonist signaling through the IL-36 receptor. J Immunol. 2014;193(2):921–930. doi:10.4049/jimmunol.1400538

34. Qin X, Liu M, Zhang S, Wang C, Zhang T. The role of IL-36γ and its regulation in eosinophilic inflammation in allergic rhinitis. Cytokine. 2019;117:84–90. doi:10.1016/j.cyto.2019.02.008

35. Magne D, Palmer G, Barton JL, et al. The new IL-1 family member IL-1F8 stimulates production of inflammatory mediators by synovial fibroblasts and articular chondrocytes. Arthritis Res Ther. 2006;8(3):R80. doi:10.1186/ar1946

36. Towne JE, Garka KE, Renshaw BR, Virca GD, Sims JE. Interleukin (IL)-1F6, IL-1F8, and IL-1F9 signal through IL-1Rrp2 and IL-1RAcP to activate the pathway leading to NF-kappaB and MAPKs. J Biol Chem. 2004;279(14):13677–13688. doi:10.1074/jbc.M400117200

37. Kovach MA, Che K, Brundin B, et al. IL-36 cytokines promote inflammation in the lungs of long-term smokers. Am J Respir Cell Mol Biol. 2021;64(2):173–182. doi:10.1165/rcmb.2020-0035OC

38. McCombs JE, Kolls JK. Walking down the “IL”: the newfound marriage between IL-36 and chronic obstructive pulmonary disease. Am J Respir Cell Mol Biol. 2021;64(2):153–154. doi:10.1165/rcmb.2020-0461ED

39. Bagdonas E, Raudoniute J, Bruzauskaite I, Aldonyte R. Novel aspects of pathogenesis and regeneration mechanisms in COPD. Int J Chron Obstruct Pulmon Dis. 2015;10:995–1013. doi:10.2147/COPD.S82518

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You breathe the air in your home every day. Unfortunately, that air may not be clean.

Every time you breathe, you could be inhaling mold, pet dander, allergens, toxins, and other airborne contaminants.

Fortunately, air purifiers are more effective than ever.

Today’s top air purifiers use proven technology to give you fresher, cleaner air in your home in minutes. Just plug the air purifier in, let it run, and enjoy a healthier environment.

We tested and ranked the world’s best air purifiers. After hundreds of hours of research, here’s what we found.

Our Rankings

All air purifiers claim to cleanse the air. However, not all of them are equally as effective.

After hundreds of hours of research and deliberation, here’s how our editorial team ranked the world’s best air purifiers.

  • Best Air Purifiers:
    • Purifair
    • Blast Auxiliary Air Cleaner
    • Blaux In Home
    • Proton Pure
    • DivinAir Dehumidifier
    • Ion Pure
    • Air Protect Pro
    • Ioner Air Purifier
    • Air Cleaner Pro
    • CleanAir S
    • Air Cleaner
    • Safe Air X
    • Air Purifier X
  • Best Passive Air Purifiers and Deodorizers:
  • Best Breathing Improvement Products:
    • The Breather
    • AirPhysio
    • Hale Breathing
    • FEND Nasal Mist
    • LifeVac

Purifair

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Purifair instantly purifies the air in virtually any indoor space with a touch of a button. It’s a quiet, filter-free, and surprisingly small device that uses negative ion technology to remove particles from the air.

We like negative ion technology because it doesn’t discriminate between types of particles: the negative ions simply attach themselves to positively-charged contaminants in the air, forcing them to fall to the ground. It’s a popular and proven air purification technology used in medical settings.

If you’re looking for a cheap, fast, and effective way to cleanse a bedroom, office, or other small space around your home, then Purifair could be the right choice.

Price: $49.99

Blast Auxiliary Air Cleaner

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The Blast Auxiliary Air Cleaner is a no-nonsense device designed to filter particles as small as 0.3 micrometers, making it effective for cleansing a range of toxins from the air.

Like other top-ranked portable air purifiers on our list, the Blast Auxiliary Air Cleaner uses negative ion technology to attract positively-charged particles and remove them from the air. However, the purifier also has an activated carbon charcoal filter for additional filtration technology.

Just turn on the Blast Auxiliary Air Cleaner, and the device starts to purify your air in seconds. It’s surprisingly quiet, and the small frame makes it easy to fit the cleaner anywhere you need – from a nightstand to a desk to any other space in your home.

Price: $69.99

Blaux In Home

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Blaux In Home is an air purifier that uses an all-in-one replaceable charcoal filter pod and an ionizing airborne particle cleaner to cleanse the air you breathe. It even has a fresh scent deodorizer to give your air a fresher, cleaner scent after the device runs.

Featuring 3 fan speeds, Blaux In Home has complementary features we don’t see with other air purifiers – including a night light at the base and sophisticated cleaning functionality.

After placing the activated charcoal filter in the unit, it can instantly start clearing dust, allergens, pollen, odor, smoke, and other contaminants from the air using proven filtration technology.

Price: $49.99

Proton Pure

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Proton Pure scrubs indoor air using a three-stage purification process, quickly eliminating up to 99.7% of indoor air pollutants.

The triple filtration system removes microscopic particles as small as 0.3 microns in size from the air, helping you enjoy a safer and cleaner indoor environment. Each pint-sized Proton Pure claims to clean 350 square feet of space, making it ideal for medium and large-sized rooms in your home.

To achieve these benefits, Proton Pure uses three filtration systems, including a mechanical filter (to catch large particles), a True HEPA filter (to remove 99.7% of all microscopic particles as small as 0.3 microns), and a carbon filter (to remove VOCs, chlorine, smoke, and other unwanted odors). Together, these three filters can quickly cleanse your home’s air.

Price: $149.95

DivinAir Dehumidifier

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DivinAir Dehumidifier is a combination of an air purifier and a dehumidifier. If you live in a humid environment, then moisture in the air can wreak havoc on your home and raise indoor temperatures.

After running DivinAir Dehumidifier with the press of a button, you can leave every corner of your home feeling dry and comfy. It offers 360-degree effectiveness, PTC heating and drying, and non-consumable silica particles for moisture absorption, among other perks.

Other air purifiers simply remove particulate matter from the air, but DivinAir Dehumidifier has the added benefit of removing moisture. It works in up to 250 square feet of space and uses heating elements with thermal conductivity to suck moisture from the air, leaving your environment feeling cooler and more comfortable.

Price: $69.99

Ion Pure

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Ion Pure is an air purification system that looks more like a portable hard drive than a conventional air purifier. You plug Ion Pure into an electrical outlet of your home, and the unit provides constant air purification without maintenance.

If you can plug a phone charger into the wall, then you can use Ion Pure to cleanse the air in your home. You can buy multiple units at a discount rate, spreading them throughout your home to provide effective cleansing power.

Each Ion Pure produces zero pollution, consumes low energy, and is made from shock-resistant ABS material for enhanced durability. The unit produces negative ions to dispel particles from the air you breathe around your home.

Price: $55.99

Air Protect Pro

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Air Protect Pro is an air purifier designed to give you clean, fresh, and safe indoor spaces with superior portability. The unit filters 99.7% of particles and helps improve indoor air quality.

Each Air Protect Pro covers rooms up to 20 square meters, or around 215 square feet. That makes Air Protect Pro ideal for everything from offices to bedrooms to medium-sized living rooms and more

Just press the button on Air Protect Pro, and the unit will start to filter the air. We also like how Air Protect Pro has active detection features: the three-level detector reflects air quality in real time, making it easy to see how healthy – or dirty – the air inside your home is and when it’s time to run the air purifier.

Price: $139.95

Ioner Air Purifier

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The Ioner Air Purifier is a portable air purifier you can wear around your neck to purify the air wherever you go. Instead of needing to plug in the air purifier or place it on a desk, you can enjoy on-the-go air purification with zero hassle.

By wearing the Ioner Air Purifier all day, you can remove bacteria, odors, viruses, and allergens from the air you breathe. You could have a lower risk of getting sick when using the Ioner Air Purifier. At the very least, the Ioner Air Purifier makes the air around you smell better.

If you want on-the-go protection against airborne contaminants and particles, then the Ioner Air Purifier could be the right choice.

Price: $59.95

Air Cleaner Pro

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Air Cleaner Pro is an air purifier that uses negative ions to eliminate particulate matter from the air. The unit also releases ozone to decompose bacteria that produce bad smells. Overall, that means you can breathe better and protect your family by cleansing the air inside your home.

Air Cleaner Pro has a unique design with four buttons. Just plug in the unit, then activate it to enjoy on-the-go charging protection.

Each Air Cleaner Pro can eliminate a significant amount of mites, pollen, smoke, and smells from the air you breathe. Instead of breathing in harmful toxins constantly, you can enjoy fresh and clean air all the time.

Price: $55

CleanAir S

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Clean Air S is an air purifier, ionizer, and disinfector that uses True HEPA H13 and carbon nano filters to eliminate toxins from the air. According to the manufacturer, each CleanAir S kills 99.9% of viruses while eliminating pollutants, toxins, and allergens from the air.

Each CleanAir S has a one-touch, easy-to-use operation while consuming low levels of energy in an ultra quiet design.

Like other portable air purifiers on our list, CleanAir S is designed to cleanse smaller spaces – not larger homes or rooms. According to the manufacturer, CleanAir S is ideal for homes, offices, bathrooms, and cars. Just place the air purifier in a central spot, press the button, and enjoy cleaner air.

Price: $49

Air Cleaner

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Air Cleaner is an appropriately-named air purification system that protects your health and combats dryness, adding humidity to the air while cleansing the air at the same time.

By running Air Cleaner daily, you can avoid flaky skin, cracked lips, and a scratchy throat. If you run an air conditioner all summer long, or if you live in a dry climate, then dryness can wreak havoc on your body. Air Cleaner solves that problem.

Priced at $55 per unit, Air Cleaner is available in multiple colors. It’s also portable and easy to charge, featuring a USB port for easy charging capability. If you can plug in your smartphone, then you can use Air Cleaner to add humidity to the air while cleansing it at the same time.

Price: $55

Safe Air X

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Safe Air X is an air purifier that makes family gatherings and social events safer. You plug in the Safe Air X unit, then track the air quality in the surrounding environment to determine if it’s safe

Safe Air X uses high-end technology to detect contaminants in the air you’re breathing – including carbon monoxide and carbon dioxide levels. If levels exceed a certain amount, then Safe Air X issues an alert.

Safe Air X also tracks the temperature, humidity, and particulate matter (PPM) in the air. If you want to see the health of your indoor air at a glance, or if you want to track the performance of other air purifiers, then Safe Air X is a must-have device.

Price: $79

Air Purifier X

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Air Purifier X is a portable fan capable of cleaning 99.9% of particles in the air. The unit uses a nearly-silent motor to purify the environment using ozone.

The fans within Air Purifier X spread the ozone particles throughout the indoor environment. Those ozone particles latch onto harmful particulate matter, helping you remove toxins from the air.

Air Purifier X features a different design than other units here; with a large fan on one side and a single button on the top, Air Purifier X is a no-nonsense device designed to give your home significantly cleaner air.

Price: $65

Best Passive Air Purifiers and Deodorizers

You don’t need electricity for effective cleansing; instead, some of the best air purifiers use activated charcoal in a bag to cleanse the air. You can place these bags in a room, a gym bag, a laundry hamper, or anywhere else for passive protection without electricity.

Each of the passive air purifiers and deodorizers listed below can help you enjoy round-the-clock protection with zero hassle or operation required.

AirJoi

AirJoi is the first air purifier on our list that works without electricity: just add the AirJoi bags to your room, car, or home to cleanse the air over time.

AirJoi works similar to baking soda, providing passive protection against odors and toxic substances. However, each AirJoi bag is significantly more effective than baking soda. It can protect against moisture, mold, and bacteria buildup and remove unwanted odors everywhere from your car to your bathroom, bedroom, laundry bag, gym bag, or closet.

Many people order multiple AirJoi bags for on-the-go cleansing throughout their home. Using micro-porous activated bamboo charcoal, AirJoi can protect your home against airborne contaminants in all environments.

Price: $19.99

PureAir Max

PureAir Max uses similar technology to AirJoi, cleansing the air using the power of activated bamboo charcoal. Just place a bag in a room, a gym bag, or a laundry hamper, then enjoy passive protection against odors and toxic buildup.

Activated bamboo charcoal works because of its unique chemical makeup. The shape of the charcoal molecule is uniquely designed to latch onto toxins in the air, which is why charcoal is a popular cleansing compound. PureAir Max uses this same technology to give you non-toxic, chemical-free, perfume-free cleansing throughout your home.

Priced at $49 per bag, PureAir Max can rapidly cleanse your home and provide ongoing protection – all without using batteries or electricity.

Price: $49

Best Breathing Improvement Products

Do you regularly feel out of breath? Do you struggle with endurance and energy throughout the day? It could be a breathing issue.

Many people have poor breathing after living in toxic indoor environments. That’s why some people use breathing improvement products to strengthen breathing, help you take fuller breaths, and enjoy a better overall quality of life.

Good breathing improvement products are proven to improve respiratory health, including respiratory health for those with breathing issues. Here are the top-ranked breath strengthening products available today.

The Breather

The Breather is a handheld device that strengthens your breathing naturally. Just place the device against your lips, breathe through it several times, and improve your breathing strength.

You can adjust the intensity of The Breather based on your desired resistance. The stronger the resistance, the more of a workout it is to use The Breather.

Recommended by doctors and pulmonologists, The Breather uses proven respiratory muscle training (RMT) technology to help you breathe easier in weeks. The medical-grade device is backed by science and has sold 1.5 million units to date.

Price: $49.99

AirPhysio

AirPhysio is a patented, award-winning device that clears mucus from your airways, helping you maintain optimal hygiene in your lungs.

Using the power of oscillating positive expiratory pressure (OPEP), AirPhysio can naturally improve your breathing. When you exhale through the device, it creates positive pressure in your lungs, loosening mucus from the walls of your airway.

Like other top-ranked breathing devices on our list, AirPhysio is recommended by doctors and pulmonologists worldwide. In fact, pulmonologists use AirPhysio daily to help with symptoms of asthma, atelectasis, bronchiectasis, emphysema, COPD, chronic bronchitis, and other conditions.

Price: $59.99

Hale Breathing

Hale Breathing opens your nasal passage to help you breathe more easily. The discreet device fits within your nose and stays there throughout the day and night, making it easier for you to take fuller breaths.

If you struggle to take full breaths, or if you find yourself frequently out of breath, then Hale Breathing could help. Described as “like a contact lens for your nose,” Hale Breathing works without toxins or sprays to clear nasal passageways.

Some people use Hale Breathing for better daily breathing. Others use it to stop snoring or improve sleep quality. Whether you have small nasal passageways or you’re trying to improve breathing in multiple ways, Hale Breathing is doctor recommended and backed by science.

Price: $29.99

FEND Nasal Mist

A single spray of FEND Nasal Mist can filter the air you breathe, removing airborne allergens, carcinogens, and pathogens before they enter your lungs.

Backed by $2 million in sales, FEND Nasal Mist is made in Germany, doctor-recommended, and backed by science. Just spray the mist around your face, and you can prevent up to 99% of allergens, carcinogens, and pathogens from reaching your lungs.

In fact, just two sprays of FEND Nasal Mist can filter the air you breathe for up to six hours. After you spray the mist towards your face, the mist particles travel precisely to your nasal passageways and throat to maximize their filtration effect, helping you enjoy on-the-go protection.

Price: $29.99

LifeVac

LifeVac is a life-saving device to save loved ones from choking. Backed by 370 saved lives and counting, LifeVac uses the power of suction to free up a blocked airway.

Ideal for use in schools, offices, and homes, LifeVac is proven to be the most effective way to help a child or adult during a choking emergency.

Just place LifeVac over the mouth and nose to create a seal, then press the plunger down to remove the lodged food or object in seconds. It can genuinely save a life in a choking emergency. LifeVac has sold over 100,000 units in 40+ countries to date, and the doctor-approved device is available without a prescription.

Price: $69.95

How We Ranked

Some air purifiers barely filter anything. Others provide medical-grade filtration. Sometimes, it’s tough to separate the best and worst air purifiers. However, we used the following ranking factors to do exactly that:

Air Purification Effectiveness: We simulated real-world environments, then rated each air purifier based on its performance. The best air purifiers filtered contaminants from the air without leaving an unusual odor or residue behind. The worst air purifiers had no noticeable impact.

Science-Backed Technology: Ozone filtration, negative ion filtration, carbon filtration, and other proven filtration technologies can genuinely remove toxins from the air. We liked air purifiers that used science-backed technology.

Transparent Advertised Effectiveness: Some air purifier companies randomly throw out claims about filtering “99.99% of particulate matter” from the air without justification. We were wary of air purifier companies that made dishonest marketing claims.

Ability to Target Multiple Particles: The best air purifiers target germs, particulate matter, smog, allergens, pollen, toxins, and other items in the air. We liked air purifiers that targeted multiple particles for maximum effectiveness.

Battery Life, Power Source, and Charging Capacity: Some air purifiers work for 10+ hours on a single charge, making it easy to carry the air purifiers around your home wherever they need to go. Other air purifiers require a constant power source – which is fine. We considered battery life and charging capacity in our rankings of some portable air purifiers, although we weren’t biased against air purifiers that required a constant power source.

Ease of Use: Did the air purifier take a while to charge? Did it have a short charging cord? Was it complicated to operate? Or did the air purifier have a simple, effective one-button design? We liked air purifiers that were easy to use.

Price & Value: You don’t need to spend $300 to get a good air purifier anymore; instead, some of the best air purifiers on our list are available for under $100. We weren’t biased against specific price points, although we considered price and value in our rankings. If you’re paying a premium price for an air purifier, then you should get a premium value. If you’re paying a budget price, then you shouldn’t need to compromise on quality.

Maintenance Requirements, Filter Replacements, and Durability: Does the air purifier last a long time? Or does it fall apart after a few months of use? Do you need to replace the filters continuously? Or does the purifier clean itself and stay effective after years of use? We considered maintenance requirements and durability in our rankings.

Square Footage of Area Covered: Some air purifiers cover 100 to 200 square feet, making them ideal for average-sized offices and bedrooms. Others cover 400 to 1,000 square feet, making them ideal for smaller homes, larger rooms, and apartments. We liked air purifiers that were open and honest about their square footage coverage.

Noise: Some air purifiers are extremely effective at cleansing the air, but they’re also ridiculously loud. We preferred air purifiers that combined effective purification with quiet operation – or at least had multiple speeds to customize the noise level. Some air purifiers had three fan speeds, for example, or a night mode for easy sleeping.

Customer Reviews, Ratings, & Real World Experiences: We tested each air purifier on our list in our simulated testing environment. However, people live in different places. The air you breathe has different humidity levels, particulate matter levels, and other features than the air we used. That’s why we also considered customer reviews in our rankings. Some of the best air purifiers are backed by thousands of five-star reviews.

Complementary or Added Features (Like Night Lights or Carrying Handles): Some air purifiers have carrying handles, night lights, and other features to expand their functionality. We primarily judged air purifiers based on their filtration technology, but we also considered complementary or added features in our ranking.

Design, Appearance, & Aesthetic Appeal: Some air purifiers look futuristic and cool. Others look bland and boring. It wasn’t the most important ranking factor, but we did consider design and appearance in our rankings. Because air purifiers are placed in visible areas of your home, you want them to look good.

Moneyback or Satisfaction Guarantee: It’s not acceptable for an air purifier company to not have a moneyback guarantee. Today, virtually all companies offer a strong moneyback or satisfaction guarantee, making it easy to get a refund on your purchase if you’re unsatisfied. We liked air purifiers with a long, flexible, and comprehensive satisfaction guarantee.

Top 17 Benefits of Using an Air Purifier

You may not think you need an air purifier. However, the world is filled with toxins, particulate matter, allergens, smog, and other contaminants.

Using an air purifier can change your life. Here are some of the benefits people use after running an air purifier:

Help Relieve Symptoms of Asthma: Many people run air purifiers to help with breathing problems like asthma. When you have asthma, you have inflamed bronchial tubes. Pollutants like pet dander, pollen, and dust mites irritate these tubes further, making it harder to breathe. By running an air purifier, you can help relieve symptoms of asthma by removing irritants from the air.

Eliminate Harmful Compounds from Indoor Environments: Many of use are breathing in toxic air without realizing it. Your indoor environment might have carbon monoxide and nitrogen dioxide particulate matter, for example, which can affect your health over time. Carbon monoxide exposure is deadly in high doses. However, studies show that even low doses of carbon monoxide over time can increase the risk of dementia and Alzheimer’s disease.

Get Rid of Vehicle Smog and Other Pollutants: If you live in a city, then your air is likely much more toxic than air in the countryside. Good air purifiers get rid of vehicle smog and other pollutants from the air, helping you breathe cleaner even in the middle of an urban environment.

Reduce the Spread of Airborne Diseases: Many diseases spread through the air. There’s a reason your whole house might get sick when one family member catches the flu. Air purifiers use HEPA filtration technology to reduce the spread of airborne diseases. A good air purifier could save someone’s life – especially if you live with older adults, children, or anyone with a weakened immune system.

Get a Better Sleep: Do you struggle to sleep at night? Do you regularly wake up? Do you snore? Air purifiers could help with all of these things. Studies show cleaner air is linked to a better night’s sleep. When you have poor-quality air in your home, you’re more likely to sneeze, cough, or feel congested overnight.

Filter Carcinogens (Cancer-Causing Compounds): The world is filled with carcinogens. Health authorities classify compounds as carcinogens if they’re linked to cancer. Some of the best air purifiers remove carcinogens from the air. Every time you remove a carcinogen from the air, you reduce the chance of breathing in that carcinogen. The fewer carcinogens there are in your body, the lower your risk of cancer.

Eliminate Hazardous Compounds and Toxins, Including Asbestos: Asbestos was commonly used in commercial and residential construction from the 1940s and 1960s. Depending on the age of your home, you could be exposed to asbestos daily. Air purifiers can eliminate hazardous asbestos particles.

Remove Pet Odors: Do you have pets? Pets leave your home with an unpleasant smell. No matter how much you clean, it’s tough to remove that smell from the air. Air purifiers use proven technology to latch onto odor-causing particles, giving your home a fresh and clean scent. Whether you have one pet or multiple pets, a good air purifier can make your home smell better than ever.

Add or Remove Humidity: Many air purifiers also double as humidifiers or dehumidifiers. If you live in a dry climate, then adding humidity to the air can help with cracked skin, wrinkles, and a scratchy throat. Or, if you live in a humid climate, then removing humidity from the air can help with mold and indoor comfort levels. Running an air conditioner constantly can dry out your home, leading to flaky and cracked skin. Good air purifiers help by adding or removing humidity.

Control Seasonal Allergies: If you regularly experience seasonal allergies, then an air purifier can help. Air purifiers remove allergens from the air. Allergens are substances that irritate your allergic response. The best air purifiers free your air from pollens and molds that could trigger symptoms.

Less Dust Accumulation: Do you dust constantly? Does dust regularly build up around your home? The best air purifiers control the rate of dust accumulation, which means you may not need to dust as frequently. Most dust is actually human skin flakes. After installing an air purifier, you might notice significantly lower levels of dust around your home.

Longer Life for HVAC Filters & Devices: Air purifiers reduce strain on your air conditioning filters, furnace system, and other HVAC appliances. A good air purifier could add months or years to the lifespan of your HVAC system.

Reduce Stress: Studies show air pollutants raise stress levels. Whether you’re exposed to indoor or outdoor air pollutants, you could have higher stress levels. Stress is associated with weight gain, high blood pressure, and other health concerns. When you run an air purifier, you could remove pollutants from the air, helping you reduce stress.

Repel Mosquitos and Pests: Air purifiers can control mosquitoes and other pests around your home. Mosquitos and other airborne insects don’t like ozone or negative ions, and your air filter may push these pests away.

Control Mold: Some homes are more prone to mold than others. Maybe you live in a humid environment. Maybe your home has poor airflow. Whatever the case may be, a good air purifier could control mold, which could save you thousands in mold remediation costs and improve your health at the same time.

Help Prevent Headaches: Do you regularly struggle with headaches at home? Airborne pollutants could increase the risk of headaches. Good air purifiers help prevent headaches by removing toxins from the air.

Boost Life Expectancy: Some air purifiers have been shown to boost life expectancy. Every time you remove airborne particles from the air, you’re preventing those particles from entering your body. Particles enter your body via the lungs, then spread throughout the bloodstream. Some cross the blood-brain barrier, increasing the risk of degenerative brain disease. When you filter the air, you cut off this problem at the source, which could boost life expectancy.

How Do Air Purifiers Work?

Air purifiers work in different ways to cleanse the air you breathe. Some use ozone or negative ion technology, for example, while others use carbon filters and other mechanical filters.

Here’s how the most popular air purifiers listed above work:

Activated Carbon Filters: Activated carbon filters use the unique molecular shape of charcoal to trap odors and particles. This carbon is activated, which means it uses a natural charge to attract particles in the air. Harmful substances are drawn towards the activated carbon, and the activated carbon tracks the particles within.

HEPA Filters: High Efficiency Particulate Air (HEPA) filters capture pollutants as small as 0.3 microns. You cannot see these particles with the human eye, but the best-quality filters capture the particles regardless. Some of the air purifiers listed above use HEPA filtration technology to target the smallest compounds.

Ozone Filters: Some air purifiers generate ozone to cleanse the air. Commonly used in commercial environments (including hotels), ozone filters create large amounts of harmful ozone to neutralize odors in a room. Some portable air purifiers use low amounts of ozone and are safe for use in any room. However, higher-end commercial ozone filters require you to leave the room during operation, then air out the room before entering. They’re some of the most effective ways to cleanse odors, bacteria, and airborne contaminants from a space.

Ultraviolet Light Air Purifiers: Some air purifiers use ultraviolet light to kill germs floating in the air. Ultraviolet light has a specific wavelength to neutralize bacteria, deactivating their activity at a cellular level. Hospitals use ultraviolet light to cleanse tools and surfaces, and today’s best air purifiers use similar technology.

Negative Ion Filters: Also known as negative ionizers, negative ion filters create particles with a negative charge, allowing them to attract and latch onto positively-charged particles in the air. Instead of breathing in positively-charged harmful particles, you can remove them from the air.

Air Purifier FAQs

Our air purifier experts get plenty of questions about air purifiers and how they work. Here are some of the answers to our most commonly asked questions.

Q: How do air purifiers work?

A: Air purifiers use science-backed technology like activated carbon filters, ozone, and negative ions to remove particulate matter from the air.

Q: What is a HEPA filter?

A: A High Efficiency Particulate Air (HEPA) filter is specifically designed to capture particles as small as 0.3 microns. It uses special technology (like tiny fiberglass threads) to capture particles in the air.

Q: Do air purifiers help with the coronavirus?

A: Air purifiers that use HEPA filters could capture particulates the size of the coronavirus, which could help manage the spread.

Q: What should I look for in an air purifier?

A: Look for air purifiers with True HEPA filtration, the right size for your targeted area, and a strong CADR rating.

Q: What is CADR?

A: Clean air delivery rate (CADR) measures the cleansing speed of the purifier. Devices with a high CADR are more effective at removing smoke, dust, and pollen. Good air purifiers have a CADR of 300 to 350.

Q: How else can I improve indoor air quality at home?

A: In addition to running an air purifier, you can improve indoor air quality by keeping your windows open, vacuuming frequently, regularly changing air filters, using exhaust fans in kitchens, bathrooms, and laundry areas, and minimizing the use of candles or wood fires around the home.

Q: How long does it take an air purifier to work?

A: The best air purifiers start to work within minutes of operation. However, you should expect maximum cleansing within 30 minutes to 2 hours of operation.

Q: Where should I place my air purifier?

A: You should place your air purifier in a central, well-ventilated area of your room. Or, you should place it close to you – like on your desk or nightstand.

Q: Are air purifiers bad for you?

A: Commercial-grade air purifiers use high levels of ozone to cleanse the air, which means you need to leave the room during operation. However, studies show most ordinary air purifiers are safe and effective for anyone to use.

Q: Do air purifiers really work?

A: Yes, air purifiers really work. The best air purifiers are backed by science to capture a significant amount of particulate matter, cleansing the air you breathe.

Q: What’s the best air purifier?

A: Any of the top-ranked air purifiers on our list are among the best available today, including Purifair, Blast Auxiliary Air Cleaner, Blaux In Home, and Proton Pure.

Q: What are the symptoms of poor indoor air quality?

A: Symptoms of poor indoor air quality include frequent headaches, illness or lethargy among pets and children, and unusual smells around the home.

Q: What is ACH?

A: Air charges per hour (ACH) indicates how frequently an air purifier filters or changes the air. The best air purifiers have an ACH of 6 to 8, which means they cleanse all of the air in your room 6 to 8 times per hour.

Q: Are air purifiers expensive to run?

A: Most air purifiers are energy efficient devices that cost only a few dollars per year to run, even when using the devices regularly.

Q: Are there side effects to air purifiers?

A: There are no known side effects to ordinary air purifiers; they’re proven to be safe and effective.

Q: How often should I run my air purifier?

A: Run your air purifier as often as you like to cleanse the air. Some run their air purifier for a few hours per day, for example, while others leave them running whenever they’re in a room.

Q: Do air purifiers help with allergies?

A: Yes, good air purifiers cleanse allergens (allergy-causing compounds) from the air you breathe, helping you deal with allergies.

Q: Do air purifiers help with asthma?

A: Air purifiers can remove particulate matter from the air, which could help with asthma. Asthma is a condition where you have inflamed bronchial tubes, and particulate matter could irritate these tubes. By removing this particulate matter, you may notice fewer symptoms of asthma.

Q: Should I run my air purifier continuously?

A: Some studies show air purifiers work best when run continuously. Generally, the more you run your air purifier, the cleaner your air will be.

Final Word

An air purifier works within seconds to improve indoor air quality. A good air purifier uses negative ions and other technology to filter the air you breathe, helping you enjoy cleaner and fresher air.

Maybe you want better sleep. Maybe you want to get rid of pet odors around the home. Maybe you want to protect your family.

Whatever the reason may be, a good air purifier could change your life every time it runs.

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Disclaimer:

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Introduction

Respiratory disorders such as chronic obstructive pulmonary disease (COPD) place a large burden on hospital budgets. Community interventions that reduce exacerbations of bronchitis, improve quality of life and reduce the need for hospital admissions and length of stay have the potential to both enhance patients’ lives and to save healthcare costs. This is particularly important when hospital respiratory services are burdened with Covid-19 patients.

In Aotearoa New Zealand (NZ) there were 61,516 hospital admissions for COPD over the 5-year period July 1, 2008, to June 30, 2013, costing $300m.1,2 When adjusted for population and inflation in medical services costs, this amounts to $83m in 2020, assuming a stable incidence rate. Like many other chronic diseases, COPD disproportionately affects indigenous Māori and Pasifika peoples.1 Healthcare providers worldwide are seeking approaches to reduce costly hospital admissions.

Oxygen administered via NHF is used worldwide for managing critically ill patients hospitalized with hypoxaemic respiratory failure, which is not always feasible using ordinary face masks or standard nasal cannulae.3 AirvoTM NHF devices (Fisher & Paykel Healthcare Ltd, Auckland, NZ) are used in Middlemore Hospital, Auckland (MMH), and increasingly across other NZ hospitals, for managing patients suffering acute exacerbations of COPD, bronchiectasis, and pneumonia. They have also gained acceptance in managing patients admitted with SARS-CoV-2 pneumonitis, so long as patients are managed in a negative pressure environment to reduce the potential for cross infection. Indeed, of COPD patients admitted to MMH, 50% received NHF and 42% used continuous positive airway pressure, which have both been shown to reduce the need for intubation and intensive care unit admission.4,5

The Airvo NHF device allows warmed and humidified air to be delivered at high flow rates ranging from 10 to 60 L/min, thus increasing the fraction of inspired oxygen from 21% to 100% depending on patient requirement. In addition it provides a modest increase in end expiratory airway pressure of 2–5cm H2O, which increases carbon dioxide clearance and diminishes the work of breathing in both acute and chronic (ie home based) stable settings.3,6–10 The clinical and economic benefits of NHF for both COPD and bronchiectasis patients in the ambulatory care setting have also been evaluated in randomized controlled trials both in NZ11–13 and in Denmark.14,15 Subsequent economic evaluation in NZ showed this intervention to be cost effective by local criteria, with a cost per quality adjusted life year (QALY) of around $NZ20,000.11

A randomized, controlled, 12-month trial of NHF in 200 patients with COPD and chronic hypoxaemia in the North Jutland Region of Denmark between December 2013 and July 2015 demonstrated reduced frequency of both non-admitted and admitted exacerbations of COPD and a lower total score on the St. Georges Respiratory Questionnaire. The average use of the NHF device was 5.9 hours per day, varying from almost nil to 10 hours. Inclusion criteria were chronic hypoxic failure (ie, three arterial blood gasses during stable conditions demonstrating hypoxemia) and previously prescribed long-term oxygen therapy (LTOT) by a pulmonary medicine specialist. Exclusion criteria were malignant disease, terminal nonmalignant disease, unstable psychiatric disease, and long-term non-invasive ventilation.14

The NHF treatment group had a predicted annual exacerbation rate of 3.12 compared with 4.95 per annum in the control group (p<0.001), adjusted for baseline rate, age, and sex. Predicted hospital admission rates favoured the treatment group (1.08 versus 1.22/patient/year, p = 0.373). In addition, for both exacerbations and admissions there was a strong regression relationship between event rate and actual number of days of use of NHF. For hospital admissions, predicted rates were 0.79 versus 1.39/patient/year for 12 months versus zero use of NHF respectively. Subsequent economic analysis of the same study reported a substantial increase in quality of life based on the St George’s Respiratory Questionnaire and when mapped to quality adjusted life years (QALYs).14

In order to estimate economic costs and benefits of medical interventions, it is both cost effective and useful to apply the findings of a clinical study to a similar patient group in another country. In this paper we report the number of hospital admissions in the treatment and control groups in the year before and after inclusion in the Danish clinical trial. We then apply current NZ costings to hospital admissions for similar COPD patients, using data derived from Counties Manukau District Health Board (CMDHB) which serves a population of 580,000. A budget impact analysis was developed from this information.

Regional oxygen budgets reside within the hospital system of care, and patients are reviewed in the outpatient clinic or from an outreach system of care. Any reduction in hospital admission rates would offset the cost of acquiring and maintaining the NHF device. Therefore, the present study takes a hospital perspective, with a focus on hospital costs and potential savings over the estimated five-year lifetime of the NHF device.

Methods

The methods of the Danish clinical trial and the characteristics of the patients have been reported in detail.14,15 Briefly, 200 patients were randomized into usual care ± NHF. At inclusion, acute exacerbations of COPD and hospital admissions one year before inclusion, modified Medical Research Council (mMRC) score, St George’s Respiratory Questionnaire (SGRQ), forced expiratory volume in 1 second (FEV1), 6-minute walk test (6MWT) and arterial carbon dioxide (PaCO2) were recorded.

Inclusion criteria were COPD with chronic hypoxemic respiratory failure (ie three arterial blood gases during stable conditions demonstrating hypoxemia). Exclusion criteria were malignant disease, terminal nonmalignant disease, unstable psychiatric disease and home treatment with noninvasive ventilation (NIV) or a change in smoking habits during the study period.15

Enrolled patients had a self-care plan with prednisone and antibiotics available. They were recommended to use the myAirvoTM NHF system with OptiflowTM cannula (Fisher and Paykel Healthcare, Auckland, New Zealand) for at least 8 hours a day, preferably at night. After titration the temperature was set to 37°C and the average flow rate was 20 L/min. Patients in the myAirvo NHF group who ceased that treatment before 12 months were nevertheless encouraged to remain in the study for all scheduled assessments and event counts.

Hospital admissions data were obtained from hospital records. Hours of usage were retrieved electronically from the NHF device.

Intervention Costs

Capital costs and running costs were obtained from the manufacturer, along with the expected lifetime of the NHF device myAirvoTM (at least 5 years). The annual cost for consumables was based on six breathing tubes, six autofill chambers, and 12 OptiflowTM nasal cannulas per year. The cost of oxygen was excluded because all patients in both groups were already receiving oxygen from an oxygen concentrator, which would be passed on to the next patient.

Exacerbations of COPD

Published analysis of the clinical study showed a substantial reduction in exacerbations, as counted via patient diaries and phone calls.14,15 However, the available information does not clarify how non-admitted patients were managed, and detailed information about the timing of these exacerbations is not available. Therefore, in order to avoid double counting and the need to impute missing data, we excluded all patient-reported information from the current analysis. This is conservative (see Discussion).

Hospital Admissions and Costs

Hospital admissions with any diagnosis of COPD were counted from Danish hospital records for a 12-month period before and after inclusion in the study. In order to apply an economic evaluation of the Danish study to the NZ context, we required the cost of each hospital admission for each patient. This information was not available from Denmark and in any case is not necessarily relevant to NZ. Therefore, NZ costs for hospital admissions were obtained from a respiratory clinic database at Middlemore Hospital for patients with any diagnosis of COPD. None of these patients had received domiciliary NHF. In selecting patients, COPD diagnostic guidelines were stringently adhered to.16,17 Thirty percent of these patients had evidence of mild bronchiectasis on computerized tomography criteria, thought to be secondary to COPD, and 54% had blood eosinophil counts of >0.3 or 3% (eosinophil count /white blood count) implying an increased risk of exacerbations, and were on inhaled steroid therapy. The average life expectancy of this patient group is around 5 years, and all patients remain on LTOT indefinitely.

Thirty patients in the clinic database who had been receiving long-term oxygen therapy for at least three months were selected to correspond to the Danish cohort. All of these patients had been admitted at least once to Middlemore Hospital in the period April 1st, 2018, to April 1st, 2020, with a total of 79 hospital admissions.

Individual hospital admission costs are based on hours of stay per hospital ward, with different costs per ward and time of day depending on staffing ratios (eg, staffing ratios are lower at night). The cost of non-admitted Emergency Department visits were not included. However, most patients with severe COPD who present to the Emergency Department are admitted to hospital. Costs were adjusted to 2020 NZ dollars (NZD) using the NZ Consumers Price Index. The mean daily cost of an individual hospital admission for this patient group was obtained by linear regression of actual hospital cost, as determined by CMDHB analysts, on length of stay.

Analytical Methods

Baseline data included hospital admission counts in the 12-month period prior to inclusion in the study. About one-third of the patients withdrew from treatment before their 12-month study period ended and some others chose to continue treatment beyond 12 months, but data on hospital admissions beyond the 12-month study length were not available. In economic analyses we assumed that the device will be passed from one eligible patient to another when it is no longer required, with a delay between patients, and that process continues until the end of the five-year lifetime of the NHF device (see Discussion). For the base case analysis we assumed 90% usage (range 85% to 95%).

Hospital admissions with any diagnosis of COPD within a 12-month period before inclusion in the clinical study and from inclusion up to the time of withdrawal from treatment or from observation (in the control group) or 12 months, whichever was shorter, were counted from hospital records.

There were 100 patients in the control group and 100 patients in the treatment group. Hospital admissions, hospital days and cost per patient were calculated for each patient. Although the patients were randomized to treatment groups, in the year prior to inclusion the average hospital cost was considerably higher in the treatment group than the control group, due to more admissions. Hence treatment comparisons effectively use the change in annualized costs from the baseline year to the study period.

All baseline data were based on one year but not all study period data were. Hence study period costs per patient were annualized by division by the fraction of a year data was observed per patient. And in summation and analysis, weighting by the length of time observed was used so the annualized data contributed in proportion to how long a period occurred, typically one year, but not always.

Although there were only two sets of measurements per patient over time (pre- and post-treatment), a repeated measures mixed model was used so the 400 data points could each be correctly weighted.

Results

Treatment

Information was available for all 200 patients in the clinical trial, 100 in each treatment group. Clinical details are provided elsewhere.14,15 The NHF flow rate was titrated at the baseline visit from 15 L/min to 20 L/min. For the majority of patients, the supplementary O2 flow rate (of average 1.7 L/min) was not altered when on NHF compared to their oxygen therapy only. Fifty-six percent overall were female, and the mean age was 70.7 years. The randomized treatment groups were well-matched clinically except for a difference in modified Medical Research Council Dyspnoea (mMRC) score.

Most (66%) patients in the NHF treatment arm of the study continued with treatment for the duration of the 12-month study period although their usage was variable. Overall device compliance, defined as the average ratio of the number of days actually used compared with the number of days before treatment was terminated, was 92%. Within the 12-month study period, the mean period on treatment or observation (truncated to 12 months) was longer in the control arm than the NHF arm (307 days vs 249 days). However, NHF patients could remain in the study after ceasing active HFNC use, and the mean study observation period in both arms was almost equal. Nevertheless, because the device will be passed from one patient to another, our calculations are based on the actual period of use.

Hospital Admissions

Fifty-five patients in the treatment group and 44 patients in the control group were admitted to hospital during the 12-month baseline period. The information available to the researchers was by ward admissions, from which hospital admissions and days per patient were derived. In the total period under analysis (including baseline year) there were 413 ward admissions with a principal or secondary diagnosis classified as respiratory (ICD10 Jxxx using international notation) and 345 hospital admissions (Table 1). Almost one-half of the ward admissions had a principal diagnosis of “COPD with acute exacerbation, unspecified” (J441) whereas J440 (“COPD with acute lower respiratory infection”) dominated in a NZ study of a previous version of the same device for patients with moderate or severe COPD or bronchiectasis.11,12 Both studies had a similar frequency of J440 and J441 taken together. Pneumonia (ICD10 J189) comprised 7.7% of the principal diagnoses of ward admissions in the Danish study (Table 1). The distribution of principal diagnoses is similar to that of hospital admissions in the CMDHB (NZ) data set: J440 + J441, 39/79 (49.4%) and J47, 7/79 (8.9%).

Table 1 Principal Diagnosis for 413 Ward Admissions in the Period 12 Months Before Treatment and During the Study Period

Adherence

In the treatment group, daily usage of the NHF device varied considerably, with 37% using it for less than five hours a day on average during the treatment period. The mean duration of treatment, as measured by the device, was 5.6 hours per day over the treatment period (median 6.2 hours). Regardless, all patients receiving the device were included in the analysis and running costs were based on average daily usage.

Hospital Admission Costs in Aotearoa New Zealand

Because hospital admission costs were not provided in the Danish study and in any case are not directly relevant to NZ, we estimated NZ costs adjusted to December 2020 NZ dollars (NZD), with data from MMH for a similar patient group.

During the period April 1st, 2018, to April 1st, 2020, there were 79 hospital admissions by 30 patients who fulfilled the criteria (see Methods). Linear regression analysis on length of stay (LOS) gave the cost per admission of:

Cost = $478 + $1234×(LOS+1) [R2 = 0.83]

Both the LOS (discharge date minus admission date) and the hospital costs in the MMH data varied considerably, with a few long stayers, as also occurred in the Danish study. The two country cohorts were comparable in mean age and average length of stay (Table 2).

Table 2 Comparison of the New Zealand Cohort with the Danish Cohort at Baseline

Hospital Admission Rates, Days, and Costs

All patients were included. Comparing the treatment period with the 12-month baseline period, hospital admission rates increased by 7% in the control group but declined by 9% in the treatment group. The annualized number of days in hospital increased by 43% in the control group but declined by 30% in the treatment group. Because of these changes, the modeled admission costs increased by 47% in the control group but declined by 26% in the treated group (Table 3).

Table 3 Hospital Admissions, Hospital Days and Admission Costs (2020 NZD) Before and After the Treatment Period Began

Intervention Costs

Because the treatment is self-administered, only the capital cost and running costs are relevant (Table 4). Setup costs for each patient, including deep cleaning, are included in the capital cost. Capital costs were amortized over 5 years at an interest rate of 5% per annum. For completeness, the cost to the household for electricity (not shown), assuming an average of 5.6 hours use per day (as measured from the NHF device) and 25c/kWh on the margin, is approximately $66 per year. Water costs are not relevant in NZ because the device uses potable tap water.

Table 4 Costs of the NHF Device Assuming Fulltime Use for 12 Months

Hospital Budget Impact

In practice there will be administrative delays between sequential patients utilising the NHF device. In the base case analysis we assumed 90% usage with zero running costs or economic benefits when not in use. There are minimal transition costs because the setup cost is included in the purchase price. Based on hospital admissions alone, and assuming that the capital cost of the NHF device ($2700) is amortized over five years at an interest rate of 5% per annum, there would be substantial cost savings due to averted hospital admissions and reduced days in hospital (Table 5). The predicted 5-year cost saving is $18,626 per device if the device has 90% usage, or $17,426 for 85% usage or $19,826 for 95% usage (Table 5).

Table 5 Predicted Hospital Budget Impact per Device Over 5 Years (2020 $NZ)

The budget impact varies considerably with the cost offset; and in the least favourable case (ie, at the high limit of the 95% confidence interval of the cost offset; see Table 3) it would cost the DHB $6118 per NHF device over a 5-year period. If the cost of a hospital admission is lower in Denmark relative to the local cost of the NHF device, the cost difference between treatment and control arms of the clinical study might not outweigh the cost of therapy. However, our sensitivity analysis showed that if the cost of a hospital admission was 20% lower there would still be a substantial cost savings over the lifetime of the device in the NZ context (Table 5). Furthermore, we showed that even an increase of 50% in the capital cost of the equipment would have only a minor effect on the cost savings. On the other hand, the economic outcome of the analysis is sensitive to the cost offset that was determined from the number of hospital admissions averted (Table 5).

In practice, the mean cost of hospital admissions for exacerbations of COPD is unlikely to be 20% more or less than that which we measured. The capital cost of the NHF equipment is realistic for the New Zealand market, although it was substantially higher for the Danish economic evaluation and it could differ across other markets.

If a decision needs to be made between purchasing the NHF device versus other hospital purchases within a given financial year, it is appropriate to discount future costs to net present value, independent of inflation. At net present value (NPV), all other variables being equal, and using a discount rate of 5% per annum, there is a predicted cost saving of $16,934 per device over its 5-year lifetime at 90% usage. In the least favourable case (ie at the high limit of the 95% confidence interval of the cost offset; Table 3), the device would cost the DHB $5562 over 5 years at net present value (Table 5).

Discussion

This is the first study to show that for sequential COPD patients receiving long-term oxygen therapy, NHF is very likely to be cost saving to the hospital budget. The cost saving to the overall healthcare budget is underestimated because the clinical trial showed a substantial reduction in exacerbations of COPD, a proportion of which were managed in the community but were not included in this analysis.15 However, self-managed exacerbations, primary care, medications and non-admitted Emergency Department visits (if any) would cost considerably less on average than the cost of a hospital admission; therefore, additional cost savings would be modest. Further, if patients were instructed to increase their use of NHF during an exacerbation they would potentially derive three specific benefits: (a) a reduction in the work of breathing (ie reduced positive end-expiratory pressure; PEEP)10,18 (b) a reduction in hypercapnia7–9,19 and (c) an increase in mucociliary clearance for those suffering symptoms of bronchitis.20 The Danish study did not attempt to amplify the positive effects of NHF by suggesting that usage be increased during exacerbations.

Findings of the clinical trial have been reported in detail previously and are not the main focus of this study.15 We have no direct information on why hospital admission rates differed at baseline or why they increased in the control group during the study period; but the increase is not unexpected because the patients had severe COPD which progresses over time. The contrast between the treatment group and control group is a strong indicator of the effectiveness of myAirvo NHF therapy, as reported previously.15

An increased need for hospitalization is a known risk factor for death for COPD patients on LTOT.21 Therefore, as shown in the control group (Table 3), it could be expected that the admission rate for the COPD cohort on LTOT would increase over time and specifically within the subgroup at highest risk of dying. The reduction in admission rates one year after starting treatment therefore is very favourable.

Our base case analysis applies to all patients who were given the NHF device, whether or not they used it as instructed. However, 37% of the patients used the device for less than 5 hours a day on average and others used it intermittently. Also, 11 patients (overlapping with the above group) discontinued therapy within the first month, some immediately. In practice, usage could be monitored for a few weeks while the patient adjusts to using the device and withdrawn if the patient is unable to tolerate it and/or is unwilling to use it. Transitioning to a new patient would be inexpensive because the cost of cleaning the NHF device and setting up for a new patient is included in the capital cost (see Table 4). Our previous analysis showed that the benefits were proportional to usage.15 Replacing a patient who underutilised the NHF device with another eligible patient would enhance both the net benefits and the potential cost savings of this therapy. Some patients were lost to the clinical study because they died, and others withdrew for various reasons including inconvenience. This does not affect the findings of our economic model, because each patient who withdraws is replaced by another eligible patient within the five-year lifetime of the NHF device.

In the base case analysis we assumed 90% usage, amounting to about one month delay between average patients. This is conservative for 2 reasons: (a) some patients utilized the device for more than 12 months, although information about their hospital admissions was not captured or included in this study; and (b) the number of patients on the LTOT register at MMH has remained constant over time, as patients who withdraw from NHF therapy are replaced by new registrants. In general, demand for the device is likely to outstrip supply. Indeed, acquisition of oxygen concentrators over the past 10 years have been provided as part of a replacement programme or to acquire more versatile concentrators (eg, capable of filling portable oxygen cylinders) rather than a need to keep pace with expanding demand. Adherence to NHF varied considerably from patient to patient. In the New Zealand context, the cost of NHF is covered by public funds and therefore is unlikely to make any difference to patient compliance.

This study could underestimate the costs at MMH because LTOT patients are severely ill and often require assisted ventilation on admission, which is not incorporated into the costs. Their average LOS is longer than average for respiratory patients and intriguingly, very similar to that of the Danish study (see Table 2).

The oxygen service in NZ and at MMH is funded by the budget for respiratory services. The service is run by specialist respiratory nurses with oversight by a designated respiratory physician. The nurses provide an outreach programme and apart from evaluating patients regularly within an ambulatory care setting are able to perform home visits when required. As above, the service could be used more often during subacute events such as in supporting patients with an exacerbation of COPD at home with further potential to reduce hospitalization. If NHF devices were available, adjustments in flow and in oxygen delivery could be made during exacerbations of COPD, which could amplify the economic impact of NHF outlined in this paper.

Study Strengths

This study, using secure hospital information without the need for data imputation or linkage, illustrates a generalisable methodology for applying clinical results from one country to budgetary considerations in another. This is much less costly than conducting an independent study. Unlike most economic evaluations of clinical trials, it considers the financial impact of the NHF device over its lifetime, with replacement of those patients who withdraw from therapy with other eligible patients. This is particularly important because of the high mortality of eligible patients. This information is valuable to hospital budget holders and decision makers.

Previous evaluation of the same clinical study, based on device use, showed a per-protocol benefit on admissions, but a comparison by randomized group (intention-to-treat) only favoured NHF non-significantly.15 However, that analysis underestimates the benefits because it counted COPD hospital admissions that occurred even after the NHF device was no longer in use by the patient.

Study Limitations

Our budget impact analysis was based on a moderately sized clinical study, in which about one-third of patients withdrew from therapy or from observation and some patients died during the 12-month study period. All risk factors for admissions, such as smoking history, were not directly considered in this economic analysis, but the trial was randomized and the number of pre-treatment admissions per patient will be a consequence of all risk factors. The study included COPD patients with a wide range of daily usage of NHF, as would be expected in real life. The economic model is based on the pragmatic assumption that the NHF equipment will be passed from one patient to another during the lifetime of the equipment; therefore, reasons for withdrawal from the study are not relevant to the economic conclusions of the study.

One limitation of this study is that it did not include the potential cost savings generated by non-admitted exacerbations of COPD.14,15 Inclusion of these would provide more cost savings, albeit mostly to the primary care budget and the household rather than to hospitals.

Inevitably, applying an economic analysis to a study in a different country with a different healthcare system is challenging. NZ data were used solely to generate costs that could be applied to the Danish study and are based on a carefully selected population of COPD patients who had been using LTOT for at least three months, as in the Danish study. One limitation of this methodology is that the NZ and Danish discharge criteria might differ. However, similarity of length of stay in the Danish study and NZ (Table 2) gives confidence that the study populations were similar.

Other Studies

While our economic evaluation was being completed, the Danish team published a comprehensive cost utility analysis of the same clinical study which included both hospital costs and primary care.14 Like our previous analysis of the same clinical trial,15 the Danish analysis was conducted as a 12-month intention-to-treat analysis14 but it did not model the pragmatic scenario of replacing one patient with another when the device is no longer being used. The Danish analysis relied on patient-specific database linkage, which is not feasible outside the country in which the trial was conducted.

The Danish analysis estimated a small incremental cost (GBP 304.4) over 12 months, with wide confidence intervals.14 In contrast, we estimate a net cost saving over 12 months of $NZ 5535 (GBP 2711), also with wide confidence intervals. The difference in means can be attributed partly to different capital costs of myAirvo in Denmark (approximately 43% higher at February 2022 exchange rates). However, the cost outcome in the NZ model is dominated by a difference in hospital admission rates and is not particularly sensitive to capital expenditure (Table 5).

More importantly, the two studies address different questions. The Danish study reported an intention-to-treat analysis of the clinical trial, during which a substantial proportion of treated patients died or withdrew from therapy for other reasons. The NZ economic model (this paper) replaces each patient who withdraws from therapy with another patient from the hospital waiting list, adjusting for equipment usage (transitional delays). There are also differences in the methodologies for adjusting for different baseline admission rates and duration of treatment. We believe that our 5-year economic model is more relevant to the practical use of NHF over the lifetime of the medical device, although it is limited to hospital admissions.

This study suggests that there is sufficient information to acquire NHF devices for the LTOT population or at the very least to conduct a Phase 4 prospective study to assess whether it is possible to improve upon the findings of the Danish study by maximizing the full potential of NHF. This could be done by providing it only to compliant patients and improving usage during exacerbations in the community. Information needs to be collected systematically to better identify those patients who exhibit obvious benefit (eg, reduced frequency of exacerbations or evidence of bronchiectasis at baseline) and to determine whether NHF used overnight whilst asleep20 leads to an improved outcome. Further, NHF may both increase the quality of sleep and also increase exercise capacity. Taken together, these benefits may increase the length of time that patients use LTOT. If such factors were apparent and were enhanced by NHF use, then they may also impact over time on mortality rates.

Conclusion

Domiciliary humidified oxygen enriched air applied through a warmed, nasal cannula to sequential patients with severe COPD has the potential to avert hospital admissions and provide substantial cost savings over the estimated five-year lifetime of the HFNC device.

Ethics Approval

Ethics approval for the clinical trial was obtained previously from the North Jutland Ethical Committee and the Danish Data Protection Agency and the clinical and economic findings have been published.14,15 The current study is based on anonymised data from this clinical trial. For New Zealand data, Counties Manukau District Health Board have advised that ethics approval is not required for this low-risk clinical audit of anonymised retrospective data. Use of New Zealand anonymised hospital admissions data also meets the expectations of the Ministry of Health for ethics approval.

Acknowledgments

Lila Prasad for providing NZ clinical data; Rosie Whittington for providing NZ cost data; William Good for assistance with referencing; Line Hust Storgaard, Ulla Møller Weinrich and Birgitte Schantz Laursen for providing the Danish clinical trial data.

Disclosure

Funding for this analysis was provided as consultancy fees to RJM and HUH by Fisher & Paykel Healthcare Ltd, supplier of the myAirvo nasal high flow device for the clinical trial. Fisher & Paykel Healthcare Ltd reviewed the manuscript but took no part in the experimental design, analysis or interpretation of the findings. RJM is Managing Director of Health Outcomes Associates Ltd. HUH is an employee and majority shareholder in Biometrics Matters Ltd. The authors report no other potential conflicts of interest for this work.

References

1. Milne RJ, Beasley R. Hospital admissions for chronic obstructive pulmonary disease. NZ Med J. 2015;128(1408):23–35.

2. Barnard L, Zhang J. The impact of respiratory disease in New Zealand: 2016 update; 2016 [cited October 7, 2021]. Available from: www.asthmafoundation.org.nz/research/the-impact-of-respiratory-disease-in-New-Zealand-2016-update. Accessed March 28, 2022.

3. Frat JP, Thille AW, Mercat A, et al. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med. 2015;372(23):2185–2196. doi:10.1056/NEJMoa1503326

4. Ni YN, Luo J, Yu H, Liu D, Liang BM, Liang ZA. The effect of high-flow nasal cannula in reducing the mortality and the rate of endotracheal intubation when used before mechanical ventilation compared with conventional oxygen therapy and noninvasive positive pressure ventilation. A systematic review and meta-analysis. Am J Emerg Med. 2018;36(2):226–233. doi:10.1016/j.ajem.2017.07.083

5. Marini JJ, Gattinoni L. Management of COVID-19 respiratory distress. JAMA. 2020;323(22):2329–2330. doi:10.1001/jama.2020.6825

6. Sun J, Li Y, Ling B, et al. High flow nasal cannula oxygen therapy versus non-invasive ventilation for chronic obstructive pulmonary disease with acute-moderate hypercapnic respiratory failure: an observational cohort study. Int J Chron Obstruct Pulmon Dis. 2019;14:1229–1237. doi:10.2147/COPD.S206567

7. Nagata K, Kikuchi T, Horie T, et al. Domiciliary high-flow nasal cannula oxygen therapy for patients with stable hypercapnic chronic obstructive pulmonary disease. A multicenter randomized crossover trial. Ann Am Thorac Soc. 2018;15(4):432–439. doi:10.1513/AnnalsATS.201706-425OC

8. McKinstry S, Pilcher J, Bardsley G, et al. Nasal high flow therapy and PtCO2 in stable COPD: a randomized controlled cross-over trial. Respirology. 2018;23(4):378–384. doi:10.1111/resp.13185

9. Fraser JF, Spooner AJ, Dunster KR, Anstey CM, Corley A. Nasal high flow oxygen therapy in patients with COPD reduces respiratory rate and tissue carbon dioxide while increasing tidal and end-expiratory lung volumes: a randomised crossover trial. Thorax. 2016;71(8):759–761. doi:10.1136/thoraxjnl-2015-207962

10. Pisani L, Fasano L, Corcione N, et al. Change in pulmonary mechanics and the effect on breathing pattern of high flow oxygen therapy in stable hypercapnic COPD. Thorax. 2017;72(4):373–375. doi:10.1136/thoraxjnl-2016-209673

11. Milne RJ, Hockey H, Rea H. Long-term air humidification therapy is cost effective for patients with moderate or severe chronic obstructive pulmonary disease or bronchiectasis. Value Health. 2014;17(4):320–327. doi:10.1016/j.jval.2014.01.007

12. Rea H, McAuley S, Jayaram L, et al. The clinical utility of long-term humidification therapy in chronic airway disease. Respir Med. 2010;104(4):525–533. doi:10.1016/j.rmed.2009.12.016

13. Good WR, Garrett J, Hockey HUP, Jayaram L, Wong C, Rea H. The role of high-flow nasal therapy in bronchiectasis: a post hoc analysis. ERJ Open Res. 2021;7:1. doi:10.1183/23120541.00711-2020

14. Sorensen SS, Storgaard LH, Weinreich UM. Cost-effectiveness of domiciliary high flow nasal cannula treatment in COPD patients with chronic respiratory failure. ClinicoEcon. 2021;13:553–564.

15. Storgaard LH, Hockey HU, Laursen BS, Weinreich UM. Long-term effects of oxygen-enriched high-flow nasal cannula treatment in COPD patients with chronic hypoxemic respiratory failure. Int J Chron Obstruct Pulmon Dis. 2018;13:1195–1205. doi:10.2147/COPD.S159666

16. Asthma-Respiratory-Foundation-NZ. NZ COPD Guidelines 2021. Wellington, New Zealand; 2021 [cited September, 2021]. Available from: www.nzrespiratoryguidelines.co.nz/uploads/8/3/0/1/83014052/nz_copd_guidelines_web.pdf. Accessed March 28, 2022.

17. Augusti A, Beasley R, Celli B; Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnoses, management, and prevention of COPD; [cited October 2021]. Available from: www.goldcopd.org. Accessed March 28, 2022.

18. Biselli PJ, Kirkness JP, Grote L, et al. Nasal high-flow therapy reduces work of breathing compared with oxygen during sleep in COPD and smoking controls: a prospective observational study. J Appl Physiol. 2017;122(1):82–88. doi:10.1152/japplphysiol.00279.2016

19. Nilius G, Franke KJ, Domanski U, Ruhle KH, Kirkness JP, Schneider H. Effects of nasal insufflation on arterial gas exchange and breathing pattern in patients with chronic obstructive pulmonary disease and hypercapnic respiratory failure. Adv Exp Med Biol. 2013;755:27–34.

20. Hasani A, Chapman TH, McCool D, Smith RE, Dilworth JP, Agnew JE. Domiciliary humidification improves lung mucociliary clearance in patients with bronchiectasis. Chron Respir Dis. 2008;5(2):81–86.

21. Soler-Cataluna JJ, Martinez-Garcia MA, Roman Sanchez P, Salcedo E, Navarro M, Ochando R. Severe acute exacerbations and mortality in patients with chronic obstructive pulmonary disease. Thorax. 2005;60(11):925–931. doi:10.1136/thx.2005.040527

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Background

Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation that is not fully reversible.1 It is associated with chronic inflammation, both locally and systemically, which increases further during acute exacerbations (AEs).2 It has been known that some inflammatory biomarkers are associated with AE,3 disease progression, and severity of airflow obstruction.4–6 Identification of these biomarkers not only provides a method of predicting prognosis but also helps with better understanding of the pathogenesis of COPD.

A key modulator of inflammation and fibrosis development, as well as tissue injury,7 fibrinogenhas been approved by the US Food and Drug Administration as a COPD biomarker for severity assessment.8 Higher baseline fibrinogen is associated with increasing incidence of COPD, COPD hospitalization, and all-cause mortality9 and related to severity of COPD.10 One study found that fibrinogen level was higher during AE of COPD (AECOPD) and returned to baseline 40 days after exacerbation.11 Fifteen-year follow-up data from the CARDIA study of 2,132 individuals showed an association between higher fibrinogen and greater loss of forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC), regardless of smoking status.12 Other studies have suggested that increasing fibrinogen levels are associated with the occurrence of COPD complications.13,14 However, there has been little research on the role of fibrinogen during AECOPD and its association with noninvasive positive-pressure ventilation (NPPV). Our study aimed to explore whether circulating fibrinogen could be used as a surrogate to measure the severity and predict the prognosis of AECOPD.

Methods

Study Design and Participants

A total of 535 patients diagnosed with AECOPD at Beijing Chao-Yang Hospital (west campus) from January 2016 to June 2021 were retrospectively enrolled in this study. The patient-selection process is shown in Figure 1. The hospital’s ethics committee determined that this study qualified for waiving patient consent according to its policies, because it analyzed a large data set without patient identifiers, which is in compliance with the Declaration of Helsinki regarding patient-data confidentiality (2016-KE-95).

Figure 1 Patient-selection flowchart.

Abbreviations: AECOPD, acute exacerbation of chronic obstructive pulmonary disease; NPPV, noninvasive positive-pressure ventilation; non-NPPV, no use of NPPV; NPPV-S, NPPVsuccess; NPPV-F, NPPVfailure.

Inclusion criteria were age ≥45 years, primary diagnosis of COPD determined by spirometry data of airflow obstruction with bronchodilator (FEV1/FVC <0.7, previous spirometry also considered, since a minority of patients had had pulmonary function tests during AE period), and admission to hospital due to AECOPD (defined as an acute worsening of respiratory symptoms requiring additional treatment). Indications for NPPV use during hospitalization were arterial blood pH <7.35 and/or PaCO2 >45 mmHg and/or presence of dyspnea at rest assessed using accessory respiratory muscles or paradoxical abdominal breathing.

Exclusion criteria were presence of other severe pulmonary diseases (such as severe bronchiectasis or pulmonary tuberculosis), end-stage chronic diseases (eg, chronic kidney failure, chronic heart failure, and malignancy) with <1 year of expected survival, requiring intubation before admission, incomplete data, and endotracheal intubation for other diseases (such as acute heart failure, kidney failure, and shock). For patients with multiple admissions during the study period, only the last was selected.

NIPPV failure was defined as worsening of pH and PaCO2 in arterial blood (defined as arterial pH <7.25 with PaCO2 increased by >20% compared with baseline or PaO2 <60 mmHg, despite maximum tolerated supplemental oxygen), clinical signs suggestive of severely decreased consciousness (eg, coma, delirium), excessive respiratory secretions with weak cough, use of accessory respiratory muscles or paradoxical thoracoabdominal movement, severe upper gastrointestinal bleeding with aspiration or vomiting, and severe hemodynamic instability despite fluid repletion and use of vasoactive agents.15

Data Collection

Baseline characteristics of age, sex, length of stay (LOS), heart rate, systolic pressure, diastolic pressure, temperature, respiratory rate, history of smoking, history of long-term oxygen therapy (LTOT), and history of domestic noninvasive ventilation (DNV) were recorded. In addition, data on comorbidities, ie, deep-vein thrombosis/pulmonary thromboembolism, emphysema, pneumonia, hypertension, diabetes, Cor pulmonale, chronic heart disease, atherosclerosis, chronic kidney disease, cerebrovascular disease, and other malignancies were collected. Arterial blood gas and peripheral venous blood (routine blood, CRP, and coagulation index <24 hours after admission) and the use of antibiotics and management of NPPV were also reviewed.

Concentration of serum fibrinogen was measured using immuno-scatter turbidimetry with a Werfen ACL Top 700. Normal fibrinogen levels are 2–4 g/L. Concentration of serum CRP were measured using immunoscatter turbidimetry with a Goldsite Aristo. Normal CRP levels are 0–5 mg/L. Parameters for noninvasive ventilation were set according to clinical practice and patients’ tolerance. An oronasal mask was used for all subjects. Arterial blood gas was intermittently analyzed by physicians according to clinical needs. When the patient reached the criteria for NPPV failure, a physician made the clinical decision (intubation or continuation of NPPV) based on laboratory data, symptoms, signs, and the inclination of the patients and their family members. The prognosis of each patient was recorded.

Statistical Analysis

Descriptive data are expressed as medians with IQRs or numbers with percentages as appropriate. Differences between groups were measured with the Mann–Whitney U test for continuous variables and x2 test for categorical variables. Spearman correlations were used for correlation analysis, and the results are displayed as correlation coefficients with P values. Multiple linear regression models were applied to identify independent risk factors of increasing fibrinogen levels. Differences in laboratory parameters among non-NPPV, NPPV-success (NPPV-S), and NPPV-failure (NPPF-F) groups were examined using the Kruskal–Wallis H test. Receiver-operating characteristic (ROC) curves were constructed to evaluate the ability of inflammatory markers to predict NPPV failure. For each ROC curve, the optimal cutoff, sensitivity, specificity, Youden’s index, area under the curve (AUC), and 95% CI were calculated. Logistic regression analyses with a conditional forward stepwise–regression model were used to determine whether any factors were independently associated with NPPV failure. All analyses were two-tailed, and differences were considered statistically significant at P<0.05. SPSS 21.0 was utilized for all statistical analysis.

Result

Baseline-Characteristic and Laboratory-Data Comparison Between Higher and Lower Fibrinogen Values

In sum, 1,925 AECOPD patients were screened and 535 selected. Among the latter, 312 (58.3%) were not managed with NPPV and 223 (41.7%) received NPPV management. Of all patients managed with NPPV, 177 (79.4%) were categorized as NPPV-S and 46 (20.6%) NPPV-F (Figure 1). In the NPPV-F group, 20 patients were intubated and 26 not, with three and 18, respectively, dying (Figure 1).

No significant differences in terms of age, sex, LOS, systolic pressure, temperature, smoking history, pH, PaCO2, HCO3, or BMI were identified between patients with low (≤4 g/L) and high (>4 g/L) fibrinogen levels. However, as suggested in Table 1, patients with higher fibrinogen (>4 g/L) presented faster heart beats and respiratory rates. There were more patients managed with LTOT and DNV in the high-fibrinogen group than the low-fibrinogen group. DVT/PTE, emphysema, pneumonia, and atherosclerosis were more commonly observed among patients with >4 g/L fibrinogen. In addition, increased CRP levels and leukocyte and neutrophil