The end stage: What is stage IV COPD?

Talking about “the end” when suffering from a disease may connote both positive and negative vibes. Positive when the end means the disease has been obliterated completely and negative when it means that the condition has reached its peak, and all hope for cure is futile. How the word is perceived in terms of medical implications vary, but what does it mean in cases of COPD?

Chronic Obstructive Pulmonary Disease (COPD) is described as "inflammatory lung disease affecting the airflow from the lungs." It has four stages –mild COPD, moderate COPD, severe COPD, and very severe COPD, which is also known as the end stage.

                                                             
                                                        Image Source: Timeinc.net

Very severe COPD is the fourth stage of the disease. Respiratory failure caused by either low blood oxygen or high carbon dioxide levels and signs of heart failure exist during this stage. This is regarded as the end stage because exacerbations may occur at least three times within the year, leading to the overall health of the patient becoming highly at risk.

Because of the various complications that occur during stage IV COPD, it is said that people die "with" their disease and not from it. Researches show that COPD is not the primary cause of the death, but other medical conditions that a patient also acquires while battling COPD. Lung cancer and heart failure are the usual medical conditions that cause death, and not COPD itself.

                                                         
                                                             Image source: Temple.edu

Studies also show that the condition of COPD may still improve even after reaching the end stage with the help of bronchodilators and corticosteroids. Continuing with proper health care, quitting smoking, and avoiding lung irritants will also greatly help in dealing with the end stage.

 Dr. Lisa Marie Cannon specializes in pulmonary diseases and critical care. For more articles about pulmonary diseases, visit this blog.

The Importance of Indoor Air Quality to Pulmonary Health

There are airborne causes behind the many diseases that affect the respiratory tract, such as the common cold and life-threatening diseases such as adverse forms of pneumonia.  Improving the air quality of a home or workplace is one of the many ways to guarantee long-term pulmonary health. 

Poor interior air quality, especially where household molds are involved, aggravates allergies and asthma symptoms.  Worse, poorly cleaned ventilation systems can contribute to the growth of airborne pathogens that lead to conditions like legionnaire's disease, which can be contagious enough to infect an entire building.  In extreme cases, buildings with abysmal air quality will develop sick building syndrome, where occupants would experience a sharp and usually poorly understood decline in health merely by being in the building.

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Improving indoor air quality relies on accomplishing three things: inhibiting the growth of bacteria and other pathogens, removing airborne pollutants and contaminants, and providing adequate ventilation.  Measures often involve keeping the HVAC system clean and free from mold and sources of contaminants.  Proper maintenance can also prevent the spread of pathogens by preventing the conditions that foster their growth. 

Other means of maintaining good air quality is inhibiting the growth of mold by maintaining  low humidity and regularly cleaning surfaces prone to mold infestation.  Yet another is placing indoor plants;  not only do houseplants contribute to the aesthetic quality of a home or office, some of them actively absorb significant amounts of atmospheric pollutants from the air.

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Dr. Lisa Marie Cannon is a pulmonologist who specializes in diagnosing, treating, and managing respiratory conditions like pneumonia.  Visit this Facebook page for more updates.

REPOST: Healthier lungs in California kids after pollution controls

A study conducted in California found better lung function among kids as the state's air quality improved.  This Reuters article provides the details.

(Reuters Health) - Doctors have long predicted that less air pollution will produce healthier lungs. Now a first-of-its-kind study of 2,120 children in southern California has documented dramatically better lung function growth as air quality has improved.

       

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Over a 13-year period, the proportion of children with poor lung capacity and lung health fell by half as levels of nitrogen dioxide and particulate matter dropped. The gains were seen both in youngsters who had asthma and in those who did not.

“It certainly supports the efforts that have been made over 40 years to improve air quality,” chief author Dr. James Gauderman of the Department of Preventive Medicine at the University of Southern California in Los Angeles told Reuters Health. “We would expect improvements in other urban centers to produce similar improvements in children’s health.”

The study, published in the New England Journal of Medicine, complements research showing that childhood lung function deteriorates and the risk of asthma rises as pollution levels rise.

"This is an association study, so there's always a question of cause and effect. Maybe these people got healthier on their own, ate better diets. You can never say it's an absolute proof," said Dr. Norman H. Edelman, senior consultant for scientific affairs at the American Lung Association.

        

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"But it's not a standalone study. It's based on older studies that show an association between the degree of air pollution and lung function in kids. This turns around and looks at improvement," he told Reuters Health.

Gauderman and his colleagues examined the long-term effects in children by studying three groups during three time periods between 1994 and 2011. Typically, the children entered the study around age 11 and were followed for four years, a period when the lungs are developing rapidly. All lived in the Los Angeles area, a region of the U.S. known for air pollution problems, which have been abating as a result of strict state controls.

“We looked at the proportion of children whose lung function was below 80 percent of normal. That’s a cutoff a physician will often use to flag a person for a possible issue with their lungs,” Gauderman said. While 7.9 percent of children fell into that category in 1998, the proportion had dropped to 3.6 percent by 2011.

“We certainly suspected that improving air quality would improve children’s health,” Gauderman said. “We were surprised by the magnitude of the effect that we’ve seen.”

"What's news about this is the large magnitude of the effect, from 8 percent down to 4 percent," said Edelman, who was not connected to research. "Asthma is present in 10 percent of the population and that's a major health problem. If a percentage of those kids is going to have worse asthma because the air pollution has limited their lung growth, that's a big deal."

During the study years, the air improved “dramatically,” Gauderman’s team writes in their report. For example, in 1994-1997, each cubic meter of air in one of the most-polluted communities, Mira Loma, had 31.5 micrograms of small particles called PM2.5 that penetrate deep into the lungs. By 2007-2010, Mira Loma averaged 17.8 micrograms of PM2.5 per cubic meter of air, a 43 percent decline. All five study sites had significant drops in particle pollution and nitrogen dioxide, they note.

Overall, average lung capacity increased by 91.4 milliliters for every decrease of 14.1 parts per billion in nitrogen dioxide. It rose by 65.5 ml for each decrease of 8.7 micrograms per cubic meter of particle pollution. Significant changes were not linked to ozone levels, but levels of that pollutant have not declined as dramatically over time.

       

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“There were significant effects on lung-function growth in both boys and girls, although the magnitude of the air-pollution effect was significantly larger in boys than in girls,” the researchers conclude.

“We found no significant association between growth in height and change in pollution during the study period, which indicates that our findings on lung-function growth are probably not the result of a secular trend in general development,” they write.

California has stricter pollution controls than the U.S. as a whole, but Edelman said even the federal clean air act has cleaned up a lot of pollution "and this study is part of that. We're making progress. There's still a long way to go. We still have much more unacceptable effects of air pollution than we should have."

Dr. Lisa Marie Cannon is a board certified physician who specializes in pulmonary care.  Visit this Facebook page for more access to resources on related topics. 

REPOST: E-Cigarettes May Not Help Smokers Quit Tobacco, Study Finds

Do e-cigarettes really help smokers stop the habit? Discover the truth from this Philly.com article below.

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While some proponents of "vaping" claim that smokers who try e-cigarettes may use them as a bridge to quitting smoking, a new study finds that the opposite may true.

The study, published April 16 in the American Journal of Public Health, found that smokers who used e-cigarettes were less likely to quit regular cigarettes than those who hadn't tried the devices.

A team led by Dr. Wael Al-Delaimy, chief of the division of global public health at the University of California, San Diego School of Medicine, followed 1,000 California smokers for one year.

The researchers found that smokers who said they had ever used e-cigarettes were about half as likely to cut down on their smoking and 59 percent less likely to quit, compared to those who never used e-cigarettes.

"Based on the idea that smokers use e-cigarettes to quit smoking, we hypothesized that smokers who used these products would be more successful in quitting," Al-Delaimy said. "But the research revealed the contrary."

Two anti-smoking experts said the study casts doubt on the notion of e-cigarettes as a smoking-cessation aid.

"These results confirm the potential harm e-cigarettes cause smokers, in that they may not only result in continued smoking but they may also discourage or delay quit attempts," said Patricia Folan, director of the Center for Tobacco Control at the North Shore-LIJ Health System in Great Neck, N.Y.

She believes that "the knowledge gap about electronic cigarettes is currently being filled in large part by e-cigarette industry advertising rather than scientific information."

But one industry representative took issue with the new study.

"Asking smokers about their 'ever use' of a product, and then somehow attributing that 'ever use' to their subsequent success or failure to quit smoking months or years down the line, is dishonest and unethical," said Gregory Conley, president of the American Vaping Association.

He said that to keep "credibility," the researchers should "have also sought out data about the relationship between 'ever use' of nicotine replacement therapy products like the gum and patch and a smoker's ability to quit."

Dr. Harlan Weinberg is medical director of pulmonary and critical care medicine at Northern Westchester Hospital in Mount Kisco, N.Y. He believes that more research on the issue is needed.

"There are no currently accepted guidelines for the use of e-cigarettes regarding smoking-cessation efficacy or as a cessation tool," he pointed out. "Their rapid use among the general population and as a social phenomenon require a more thorough evaluation regarding their safety and effectiveness."

Study author Al-Delaimy concurred. "We need further studies to answer why [smokers using e-cigarettes] cannot quit," he said. "One hypothesis is that smokers are receiving an increase in nicotine dose by using e-cigarettes."

Over the past two years a number of leading medical groups, including the American Heart Association, the American Cancer Society, the American Society of Clinical Oncology and the American Medical Association, have called for increased regulation of the sale and advertising of e-cigarettes, citing health concerns.

Dr. Lisa Marie Cannon is a licensed physician specializing in pulmonary care. Discover more information on internal medicine and pulmonary health from this Facebook page.

REPOST: Enhancing and Inhibiting Autophagy in Lung Disease is Double-Edged

According to this article, understanding the role of this double-edged-sword hypothesis of autophagy in pulmonary diseases will help in the development of personalized therapies to treat pulmonary diseases. 

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Researchers from the Weill Cornell Medical College and New York-Presbyterian Hospital in New York recently discussed the role of autophagy in lung diseases in a study titled “Autophagy in lung disease pathogenesis and therapeutics,” recently published in the journal Redox Biology.

Autophagy is a physiological process that deals with the destruction of cells in the body. It helps maintain homeostasis or normal functioning by protein degradation and turnover of destroyed cell organelles for new cell formation. In the most common form of autophagy, cytosolic materials (the fluid component of cytoplasma) are sequestered into double-membrane compartments called autophagosomes, which subsequently fuse to lysosomes where their contents are enzymatically degraded.

Recently, autophagy gained attention in human pulmonary diseases, both as a modulator of pathogenesis and as a potential therapeutic target. Studies suggest that the autophagic clearance of mitochondria, a potentially protective program, may worsen the chronic obstructive pulmonary disease by activating cell death programs.

In the review, researchers and coauthors Setfan Ryter and Augustine Choi stated that autophagic clearance of cilia components could contribute to airway dysfunction in chronic lung diseases. In certain diseases such as pulmonary hypertension, autophagy may offer protection by modulating proliferation and cell death. In other disorders, such as idiopathic pulmonary fibrosis and cystic fibrosis, impaired autophagy may contribute to pathogenesis.

The authors point out the multiple functions of autophagy and its selective autophagy subtypes may be of significance to the pathogenesis of human disease, with an emphasis on lung disease and therapeutics. In chronic obstructive pulmonary disease (COPD) for example, autophagy modulation can be observed in lung macrophages, bronchial and epithelial cells upon CS exposure and in the lungs of COPD patients, with recent studies suggesting that autophagy promotes lung epithelial cell death, airway dysfunction, and emphysema in response to CS exposure in vivo.

In certain diseases such as sepsis, autophagy may provide a pro-survival advantage by promoting bacterial clearance, and by modulating inflammation. In cigarette smoke exposure models, evidence showed an amplification of disease process when autophagy or mitophagy is activated. Currently, compounds that can modulate autophagy include the mTOR inhibitor rapamycin (an inducer of autophagy) and chloroquine or hydroxychloroquine (inhibitors of autophagy).

As the authors discussed in their review, autophagy has the ability to cause contrasting effects, indicating that a complete understanding of the pathogenic process and the impact of autophagy would be prudent before attempting to modulate autophagy in the context of human disease.

Lastly, a better understanding of the multiple pathways of selective autophagy and their impact on disease pathogenesis may also facilitate the design of more specific therapies for the treatment of pulmonary diseases, and other related diseases where autophagy may contribute to pathogenesis.


Dr. Lisa Marie Cannon focuses on diagnosting and treating patients with sleep disorders. Visit this blog for related articles and news.

An ounce of prevention: Vaccinations can prevent serious lung diseases in adults

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Many adults mistakenly believe that they no longer need vaccinations to protect themselves against certain preventable diseases. However, vaccinations can actually prevent the onset of two potentially dangerous lung diseases: pneumococcal pneumonia and influenza.

Pneumococcal pneumonia is a lung infection that, if left unchecked, can lead to more serious conditions such as meningitis, bacteremia, and even death, particularly among older adults. The disease is caused by the Streptococcus pneumoniae bacteria and can be transmitted through airborne droplets.

Common symptoms of pneumococcal pneumonia include fever and chills, difficulty breathing, chest pain, and cough.

Influenza, commonly called the flu, is a contagious illness caused by a variety of flu viruses. Although most people who contract influenza usually recover within a few weeks, some people will develop serious complications such as pneumonia and bronchitis. People with weakened immune systems, such as individuals with HIV and organ transpant patients, older adults, pregnant women, children, and people with chronic illnesses are at a higher risk of developing these complications.

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Treatment for both pneumococcal pneumonia can be very time-intensive, involving various tests, medication, bed rest, and even hospitalization.

To prevent pneumococcal pneumonia, the Centers for Disease Control and Prevention (CDC) recommends the pneumococcal vaccine, especially for individuals 65 years old or older, have a long-term health condition, low resistance to infection, and are Alaskan Natives or a Native Americans.

For influenza, the CDC recommends that individuals over the age of six months get a flu shot once every year. The vaccine is seasonal and differs from year to year, to account for the highly variable influenza virus. The vaccine comes in traditional, high-dose, intradermal, and egg-free variants, and also comes as a nasal spray.

Those considering getting either the pneumococcal pneumonia or influenza vaccine should speak with their health care provider for more information on its risks as well as its benefits.

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Lisa Marie Cannon, MD is a pulmonary disease specialist in New Jersey. Like this Facebook page for discussions on lung disease vaccinations.

REPOST: Idiopathic Pulmonary Fibrosis: Patient Needs, Perceptions and Experiences

What is Idiopathic Pulmonary Fibrosis (IPF) and how does it affect the quality of life of the patient? This article shares that understanding the difficulties that people with Idiopathic Pulmonary Fibrosis (IPF) experiencing may help healthcare providers give a better support for these patients and might improve their quality of life. 

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A new study provides improved understanding of the challenges faced by people with Idiopathic Pulmonary Fibrosis (IPF) and their caregivers, which could help in the development of supportive care and could also improve quality of life in people afflicted with IPF. The study appeared December 23rd, 2014, in the Journal of Advanced Nursing.

IPF is a progressive lung disease. Once diagnosed, individuals with IPF live on average between 2-4 years. Pulmonary fibrosis (PF) is characterized by thick, scarred tissue of the lungs, causing difficulty with breathing. In spite of the recent FDA approvals of Ebriet and Ofev in October, there is no cure, few medications currently exist to treat it, and lung transplant is often the only viable option.

Very few studies examining life quality and patient experiences exist that focus on IPF, unlike in the lung cancer literature. Such studies are greatly needed to help improve patient care.

Researchers at the University Hospital of South Manchester NHS Foundation Trust, Manchester, UK sought to better understand how IPF impacts patient quality of life. This was a qualitative study that took place from 2007–2012.

Led by Annette Duck, they studied seventeen patients with a diagnosis of IPF at a respiratory and lung transplant center in North West England. The patients were being treated by a multidisciplinary team of healthcare professionals and had moderate to advanced disease severity. The researchers also interviewed six of the “informal” caregivers for these patients.

Interviews were recorded and based on a guidebook developed by the research group. They transcribed the interviews word-for-word and used a technique called “Framework Analysis” to extract the data. Framework analysis is a systematic technique for analyzing qualitative data, particularly in teams conducting healthcare research.

The research team identified three primary themes expressed by the patients based on their interviews: 1) Struggling to get a diagnosis, 2) Loss of the life I previously had and 3) Living with Idiopathic Pulmonary Fibrosis. According to the study authors “Patients reported struggling to get a diagnosis and coping with a life-limiting, rapidly progressive illness with no good treatment and few support structures.”

The authors further stated that “Participants in this study struggled to get an accurate prompt diagnosis. They experienced functional limitation, rapid disease progression with limited support and few positive treatment options. Participant stories centered round loss of sense of self, the life they had and the person they were. Learning to live with IPF was a struggle, with increasing dependency on partners and specialists. Oxygen became a lifeline to many and helped them to feel ‘in control’.”

The study provides a comprehensive view of how IPF impacts the life and personal perceptions of people with IPF. Understanding of these findings may assist healthcare providers in providing better support for these patients and in improving their quality of life.

Dr. Lisa Marie Cannon is a physician based in New Jersey who is specializing in pulmonary disease, critical care, and sleep medicine. Like this Facebook page for more updates.