Emphysema: the disgusting word

A simple metaphore

… let’s say a bubble wrap. Many bubbles to increase the surface for contact. It’s not a flat surface but many short cylinders made of the same material. When a mini-cylinder is pressed with a the finger, the pressure increases and broke it out. What stays there is not useful as it was before. The surface is reduced after each small air-full cylinder is broken out.

When cigarette smoke enters into the airway, there’s a local reaction. Contraction of muscles around the airway (neck of a bubble) accompanied by irritation. When this reaction is repeated some air is trapped at the most internal levels of the lungs. There, many bubbles (alveoli) were available for gas exchange. The trapped air increases the pressure inside the bubbles and break them out one after another. The surface for getting most of the oxygen from the inspired air is progressively diminished.

Destroying a building: the lung

It is not only the increased pressure what breaks the bubbles out. If the plastic is weak the process is easier. The similarity implies a local response at cells of the alveoli as well as on the system of attachments. As in a building, many materials are involved in the stability of the whole structure. The system for stability of the alveoli inside the lungs is debilitated as part of the reaction to the components of smoke. Many cells come to help but the response is exaggerated and alveolar destruction also occurs.

Emphysema

When a combination of extreme local pressure and debilitation of the alveoli occurs, what comes is emphysema. Emphysema is more a histological concept, it is not based on clinical findings. For example we can say that chronic bronchitis is cough with sputum production for more than three months during two consecutive years. Emphysema is destruction of alveolar septa (divisions or walls of the bubbles), something that can be seen under microscopy.

Diagnosing emphysema

Of course it’s not required to perform a biopsy to diagnose emphysema. Usually the diagnosis is an assumption based on changes at a macroscopic level: exaggerated chest size (particularly from back to front) or chest X-rays showing localized or generalized darkness due to lost of the tiny divisions in the pulmonary tissue. When those big findings are present in a patient with history of smoking and less phlegm during coughing but with increased breathlessness when performing some physical activity, the diagnosis of lung emphysema is obvious.

Reducing the impact of emphysema

Building back the bubbles in the lungs is as easy as trying to do that with the wrap: impossible. However some interventions may help to reduce the impact of the damage. The first measure is avoiding the injure: quit smoking to protect the healthy bubbles. The second is the administration of drugs to release some trapped air. The third intervention should be decreasing the inflammatory reaction when it happens like during repeated exacerbations. The fourth is learning to use the existing saved bubbles and, finally, sometimes it may be used surgery to eliminate extensive areas where alveoli are already destroyed (this as a last minute intervention with strict criteria). Oxygen may be required when the remaining healthy surface is really small.

Emphysema or Chronic Bronchitis

Some smokers develop more emphysema than chronic bronchitis. Others tend to do exactly the opposite but most of COPD patients have a combination of both disorders.

Emphysema sounds as a very disgusting word, but it needs to be taken into account when informing COPD patients about the reality of the disease. It may sound terrible but some times is a reality to be communicated to be sure of the understanding of COPD as a serious clinical condition.

Seriousness of emphysema

We physicians can deal with more of the disorders generated by smoking cigarettes. Although emphysema is irreversible, the condition that push toward a deterioration can be controlled. Emphysema could be consider as a word to help realize of the seriousness of COPD. It’s always there in a less or more extent, but it is there. It is not that Chronic Bronchitis is better than emphysema. Both are equally relevant to the quality of life as well as a prognostic factor for the survival of a patient.

Hopefully, many investigators are working to find the actions required to reduce the impact of emphysema. It is still in the mind and hands of a patient (literally) to take the first steps against emphysema advancement.

Patient-Physician communication addressing a physical exam

At the medical office there’s a need of a dialogue.

Dialogue between patient and physician

The dialogue between patient and health care provider should be based on the potential expectations of the patients, the level of knowledge, the individual variables, the respect for the patient time, and a consideration of the power of the patient. The respiratory patient usually bases his or her visit in on the interference with the ventilation of the lungs as well as new symptoms. All this information can be gotten through the appropriate partnership built in a few amount of time. However, it is more than time what defines an adequate approach during the assessment of a respiratory patient. It’s related to straight and high quality communication.

Communication: the big deal

In the construction of a patient-physician relation, the communication needs to overlap several processes to make of them a continuum. Sending is a key element in the messaging of information to a patient. But sending is not an exclusive process, the process of delivering information to a patient requires to expect a feedback, a series of immediate reactions. The reactions of the patient come to the physician in different ways, words, facial expression, gestures, silence. It’s responsibility of the physician to give value to the patient’s reaction and preparing more support. This specific details make of the typical sender a formal receiver, while the patient is a sender.

As always, our major feature as human beings is our main problem most of the times: verbal communication. This indicates a necessity of being constantly careful when talking to the patient or the physician. I my physician clear about what I do feel? Is my patient getting the right message? If no: why?

Fundamentals of diagnosis and treatment

An appropriate diagnosis is pending on precise information and adequate analysis. If a patient gives clear messages, the physician organizes a better approach. If a physician provides with clear definite recommendations and well designed instructions, a patient is put in the right track.

Part of the communicative procedure is also supported by a physical contact integrated to the conversation. It’s more than writing on the laptop while hearing answers to those cold medical questions. A close appropriate contact with the patient during the physical examination is not only the auscultation of the thorax but asking questions and hearing the patient.

Physical exam abridging the path to diagnosis

The physical examination is mostly oriented by the answers to specific questions. Is you mass sensation at the right side? implies a careful examination of the left and later of the right side. Is the pain more intense on the back or in the chest? Imposes a starting at the less painful location. All this to create a parameter for comparison.

Of course, the intention wouldn’t be to tell to the examiner what to do but how to do it. The examiner will make a general evaluation, but this will be followed by a confirmatory process to grade the level of symptoms impact on physical structures.

The indispensable patient voice

One thing is clear: what patient says is key for exact diagnosis and efficacious treatment. Then, in first visits, the physical exam should be a good complete one. The following exams should be directed to the abnormalities informed by the patient during the visit. This does not preclude an exclusion of complete exam if it is performed very infrequently.

Then, it seems to be clear that the skills of a physician need to be put into practice combining the information coming from the patient as well as knowledge and respect. If some of this elements are not working, the decisions are far from being well oriented.

Call to a synchronic action

Patients should prepare their conversation with doctors. Doctors should be prepared to hear patients and share with them the knowledge to improve the results of an office’s visit. This will lead to a smooth process of understanding of the parties programming the cure or the approach to handle the health condition.

 

Oxygen as a drug in some respiratory diseases

Oxygen is a key element for our body to work properly. All the effort of breathing is made to keep the levels of this gas in the appropriate range. The healthy human being does not realize of the physical breathing process as a routine when the entire body is working in the positive balance of oxygen taking. However a challenge to the environment is accompanied by an increase need in oxygen so our muscles can work for running away, jumping, cycling, climbing stairs quickly, making strides, etc.

Oxygen as a excess requirement

Respiratory ill patients like those with pulmonary fibrosis, chronic obstructive disease and asthma, pneumonia, rib fractures, etc. have a diminished surface to exchange oxygen and CO2 with the atmosphere. Although the surface for exchange may be big enough to favor CO2 release, some times oxygen will not find sufficient permeable tissue to get into the blood. That’s the reason why some patients must need supplemental oxygen and others may have a delayed requirement.

Lower level of activities acting as indicators

The respiratory imposed condition may not wait for for typical exhausting tasks to add symptoms or make the reduced level of oxygen more diminished. These diseases may make the oxygen need more apparent when getting up, walking, carrying a bag with groceries, or taking a shower. For some patients, just lying on bed may reduce the surface for exchange due to obesity, diafragm weakness, occlusive upper airway (as in sleep apnea/hypopnea) or enlarged heart (just some examples).

Basement of Oxygen prescription

To indicate oxygen therapy, physicians base their decision on objective oxygen measurement that may be non-invasive or invasive. The non-invasive procedure is the Pulse Oxymetry that assesses only oxygen through the skin. The invasive procedure implies a blood sample taken from an peripheral artery (with blood coming from the heart after taking oxygen from the lungs). With the measurement of Gases of Arterial Blood it comes also the levels of CO2, as well as HCO3, and pH (among other values).

Once the reduced arterial blood oxygen level is confirmed low (hypoxemia), the election is made. Of course the supplemental oxygen is not administered to correct hypoxemia only. The oxygen therapy is started to decrease the intensity of symptoms and to reduce the workload imposed to the cardiopulmonary system when it is trying to get its best for maintaining oxygen in the best range.

Oxygen Therapy Precautions 

The oxygen therapy has potential complications although it is clearly indicated. It needs to be re-assessed on a regular basis to avoid the complications. When the right level is reached re-assessments are less frequent.

One of the most feared complications of oxygen therapy is depression of ventilatory centers (chemically confused due to the new excessive amount of oxygen supplied). Unfortunately it may appear in patients with more requirement of oxygen like those with elevated CO2 levels. This tends to appear in the most serious cases of hypoxemia: advanced stages of COPD, severe persistent asthma, obstructive sleep apnea.

When the inspired fraction of oxygen is increased over the normal atmospherical level, there’s a described risk of atelectasis (colapse of lung units where the oxygen is taken). Other risk is oxygen toxicity.

Oxygen Toxicity: special chapter

Oxygen toxicity occurs due to its chemical effect on a cellular level. This excessive oxidation leads to death of cells where the impact occurs. Actually, this effect is correlated with time of exposure and what happens is an inflammatory reaction. First with the irritating action may appear the inflammation of the trachea and bronchi with middle chest pain. Then it may be followed by reduced lung space for exchange, rigidity of local tissues, altered balance of oxygen between air and blood, hypoxemia during exercise, and reduced diffusing capacity of gases that leads to CO2 retention and no oxygen is taken.

All this occurs while the injure is being established with lession of capillaries, swelling of the lungs, and cellular destruction.

Amount and Time

As the levels and time of continuous exposure represent a risky situation, the prescription of oxygen is regulated in terms of Liters of Oxygen and hours of exposure. This needs to be clearly communicated to patients with oxygen therapy and care givers to avoid toxicity and imbalance in blood gases that may lead to confusion at respiratory centers, for instance in the Central Nervous System, with CO2 retention and worsening hypoxemia.

Oxygen may be considered a drug as it has been described with biological effects and benefits as well as potential adverse effects and events that imply warnings and precautions.

Long term Oxygen Therapy in COPD

Patients with COPD have necessary long term supplemental oxygen indicated when they have severe COPD and arterial oxygen levels less than 7.3 kPa (55 mm Hg) with or without CO2 retention or if they have arterial oxygen levels in the range of 7.3 kPa to 8 kPa (60 mm Hg) with evidence of pulmonary arterial hypertension or peripheral edema (swelling) and increased red blood cells (also called erithrocytosis, erithrocythemia more appropriately, or polycithemia) as an exaggerated response to chronic reduced arterial oxygen.

A summary

In summary, respiratory conditions may reduce the oxygen in the circulating blood. This implies that some patients may require supplemental oxygen administration. In those patients, oxygen may be required for better performance of a wide range of physical tasks. Oxygen may be injuring if given in high amounts and for extended periods of time. The administration may be required for short or long periods of time and is based on body levels of oxygen.

Previous steps?

This may be a reason to think more about Pulmonary Rehabilitation when considering to adapt to some chronic respiratory conditions.

The bad music of respiratory symptoms

The engagement of the respiratory patient in the management of their disease helps to get more success from it. The respiratory system seems to be so obvious that many people forget to ask for more facts. If a patient has acute or chronic onset disease, the questions may vary but the interest should be the same because the own health is still health.

What is a respiratory symptom?

Respiratory symptoms are the set of complaints mainly located in the respiratory tract. They may be due to local reactions at the upper or at the lower respiratory area. Some of them may have an undefined origin but most of them are clearly related to a more precise topographic area.

Up-up and away

Sneezing, nasal itching, epistaxis (nasal bleeding), nasal congestion (stagnated nasal phlegm), snoring, dysphonia, hoarseness (with breathy or harsh voice), stridor (a high pitched sound with each breathing), and throat pain are associated with diseases of the upper respiratory tract.

Everybody is going down

Cough, sputum, thoracic internal pain, breathlessness, blood tinged sputum (hemoptoic sputum), cough with blood (hemoptisis) are more signals of alteration in the bronchi and lungs.

Cough is some times misunderstood because is a symptom with a complex mechanism. Often it may be associated to upper or to lower respiratory diseases. Several circumstances may preclude an association to both segments of the respiratory tract.

Last night I didn’t get to sleep at all

Symptoms may be organized according to their chronological appearance or at least we physicians try to do that. It’s great when a patient comes with a well organized information and says (for instance): “I started with nasal congestion 3 days ago, then it appeared the cough (dry at the start and with sputum later), followed by thoracic pain at my right side which is the reason why I come today”…

Hard to say I’m sorry

When the respiratory symptoms are accompanied by non-respiratory symptoms, these may be taken into consideration. For instance: fever and weight loss are key indicators of a more complex condition and how they occur really help to clarify the diagnosis or assess the evolution (progress or deterioration).

We go together

Then in the assessment of the respiratory patient we look for local and constitutional symptoms, with the type of onset (acute, sub-acute, or chronic), as well as the evolution in the time.

Keep in mind all the symptoms and their characteristics to ease a diagnosis and appropriate management.

 

Heart defining intensive care for lungs in COPD

One of the major fears in the management of COPD is the potential need of admission to the Intensive Care Unit. The reason is the difficulty in weaning from ventilatory support that very severe patients may develop during the ICU stay. Ventilatory support at the ICU sometimes is very particular in these patients. They may have already adjusted their body to chemical changes in terms of arterial gases.

Acute exacerbation of COPD in ICU

Predicting which patients may require ICU seriously is a challenge. In an issue of Chest (Chest 2008;133:1088-1094) a team from the Department of Internal Medicine and Clinic for Pneumology and Respiratory Cell Research at the University Hospital Basel, Switzerland tested the hypothesis about a marker of cardiac stress as predictor of ICU admission requirement due to acute exacerbation of COPD (AECOPD).

BNP in the heart of COPD

The marker was the B-type natriuretic peptide or BNP which is mainly released from the heart to control different functions related to the adjustment of the body to a damaged heart.

In AECOPD is expected the sudden reduction in the oxygenation due to abrupt insults to the lung. The decreased oxygen (hypoxemia) leads to a heart response to try to support the rest of the organs. According tho D. Stolz and colleagues, the hypoxemic constriction of the vascular pulmonary bed could be paramount in the increased cardiac work. Then, the release of BNP from the heart may be an indicator of potential bigger deterioration of patients with AECOPD.

In their single centered trial of 208 patients wit an AECOPD presenting to the ER, they found that levels of BNP were significantly elevated when compared to the recovery phase of the episode.

A research found…

A total of 9% of patients with AECOPD required ICU treatment to receive mechanical ventilation and cardiovascular intensive management. These group of patients had higher values of BNP.

One of the most interesting findings was that lung function (measured through FEV1) was not correlated with BNP levels. This fact points to a more complex reality of staging systems of COPD. Maybe having a less severe disease does not exclude the possibility of being admitted to ICU, but the general status of the patient (including the cardiac state).

Taking the heart in mind

Although cardiovascular events seem not to be the predominant dangerous factors in AECOPD with fatal results, they need to be under the scope when considering the severity of AECOPD. The cardiac status may define the need of ICU in most COPD patients with exacerbations. One point is clear: exacerbations are more frequent in advanced stages of the disease when the cardiac health may have been injured especially when diagnosis is made late.

There’s no such a “curse” of COPD.

Front line and the restaurant signal

Patients with COPD diagnosis don’t start with the diagnosis. In fact, they start early in their disease without realizing of it (with their “smokers cough”). Although the main trigger for development of the disease is the exposure to the irritant, the first reaction is the self protection of the lungs: “Do not smoke” (like in the restaurant) here and then you start to close the door (Your lungs close the door reducing the size of the opening). In terms of lung function this is bronchospasm, airflow limitation, airway obstruction, or bronchoconstriction. All these terms imply the main natural response of our body: safety of the organ (protecting the organ). Smokers also develop a cellular and biochemical reaction to keep warning us of the damage in which we incur.

Many ways to describe a progressive disease

Many authors have described the string of events in different ways. Some of them point out to a downward spiral of decline, others indicate the clinical course of COPD, or the progression of the disease, natural evolution, natural history, vicious circle, etc. I feel challenged to entitle it as the “progressive decline of untreated COPD”.

Untreated and undertreated patients start with a congenital signal. Apparently, not easy to recognize until the effects are manifest, the susceptibility to environmental pollutants and mainly cigarette smoke comes with us since we are born.

A short scheme

When the subject smokes regularly the imbalance in the normal tone of the muscles surrounding the airways is lost. The net effect is the increased tone and subsequent contraction with reduced airflow, especially during the expiration. This is intensified during moderate activities when our organism requires more breathing. The respiratory impairment will be visible due to the air trapping and hyperinflation and the patient will complaint of dyspnea, followed by less activities, sedentary lifestyle, more dyspnea with minor activities, until the untreated patient feels isolated with a very reduced quality of life.

A curse for all?

However, this is the course of untreated or undertreated patients not the “curse” of a well treated and attended COPD patient. A well treated and attended patient should also be self-engaging in the management of their disease. A COPD patient shoudl get interest in their disease, playing an active role, looking for opportunities in their participation, assessing themselves in terms of benefits obtained, of deleterious effects, positive changes in their lifestyle.

Happy world

Physicians love those patients, because they consider those patients an expression of their intervention. Physicians get more involved and positive in the management of patients who respond to recommendations, teachings, as well as patients who provide with results or ask key questions.

Patients who talk to the Respiratory Therapist, to the nurse practitioner, or tho the Physician Assistant, will get the right information. The level of information about the disease for each patient should be self controlled if they don’t want to get confused. With so many sources of information, the patient need to be sensitive and particular and should be oriented by the medical team.

Don’t worry, get well

If you’re a COPD patient get out of the “downward spiral” and participate consciously in the management of the disease. If you are a member of a team supporting a COPD patient, lend a hand and get them in the right track soon. Everybody could be happier sooner reverting any “curse” from around.

More differences between COPD and asthma

According to Peter K. Jeffery, there has been some difficulty distinguishing COPD from asthma. The main reason is the occurrence of patients who have some reversibility in their airway obstruction having COPD and patients with asthma whose airflow limitation is more fixed. Some other patients may also have COPD plus asthma.

The key obstructive features in COPD

The main conditions contributing to obstruction in COPD are: Chronic bronchitis, emphysema, and chronic bronchiolitis (affecting small airways of less than 2 mm in diameter). As the airway in chronic bronchitis is inflamed, this feature leads to more difficulty in getting the diagnosis of COPD from presumptive patients with asthma  (where inflammation is a key component).

The easy difference

What seems to be clear is the main risk factor for developing COPD: the long-term exposure to inhaled noxious gases and particles, having cigarette smoke accounting for more than 90 percent of cases. In some circumstances the inhalation of smoke different to that from cigarettes (e.g. burning of wood during cooking) represents an important cause of COPD.

A key clue to have also in mind is that all smokers don’t develop COPD. It is considered that 10 to 20 percent of heavy smokers will become COPD sufferers. This indicates the relevance of some individual susceptibility to cigarette smoking. Unfortunately, there are different diseases that may appear in those who don’t develop COPD: lung cancer, cardiovascular conditions, etc.

Everybody exposed to some irritants will have a local response in the lungs. The inflammatory response seen in COPD patients is in fact an exaggeration of what is seen in everybody who inhale the irritating cigarette smoke.

Trying to target inflammation in COPD

Inhaled corticosteroids (ICS) are being prescribed for COPD. However, spirometric evidence of benefits in patients with a clearly defined diagnosis of COPD is still lacking. This is absolutely different in patients wit asthma, where the outstanding response to inhaled corticosteroids is amazing.

These findings lead to claim steroid resistance in COPD inflammation. However patients in advanced stages of COPD and with frequent exacerbations have shown beneficial effects of ICS mainly reducing the exacerbation rate.

Then, why is it so beneficial to use ICS in asthma and not in COPD? One of the reasons is that the predominant inflammatory cell type as well as the precise site of inflammation in both conditions are different.

The structural differences between COPD and asthma

While COPD airflow obstruction tends to deteriorate progressively, in asthma it occurs in a variable mode. Post mortem findings in COPD include excessive mucus and emphysema but in asthma emphysema is not a frequent finding.

The sputum of patients with asthma is crowded with eosinophils while neutrophils are more seen in COPD. The surface of the airway in asthma is deteriorated with fragility an loss of epithelium and the changes of bronchiolar mucous cells is still under debate in asthma.

COPD lungs have metaplasia and hyperplasia of bronchiolar mucous cells and the fragility of the surface epithelium is undetermined.

Some other differences between COPD and asthma have been seen in the reticular basement membrane (which tends to be thickened in asthma), local edema (also more more typical for asthma), bronchial smooth muscle (enlarged in small airways in COPD and in large airways in asthma), and bronchial glands (no change in mucin histochemistry in asthma but increased acidic glycoprotein in COPD).

Finally, the cellular infiltrate and the cytokines profile is different between both conditions: more neutrophils, CD8+ T-cells, and macrophages in COPD. In asthma, eosinophils, CD4+ T-cells are increased particularly in large airways.

For more details about COPD structural changes comparison with asthma, Peter K. Jeffery’ s review in Thorax is a good source (Thorax 1998;53;129-136)

Looking for inflammation in COPD

The confusion between asthma and COPD seems to be bigger than expected. Unfortunately, some patients are being told they have asthma when in fact they have COPD. Moreover, sometimes it’s not easy to point out to a difference. This also leads to inappropriate therapies for the right patient. Looking for clues may be difficult and some researchers are finding results.

Systemic Biomarkers of inflammation in COPD: under scope

Don D. Sin and colleagues recently published their results on the effects of a combined therapy in COPD on systemic biomarkers of inflammation (Am J Respir Crit Care Med 2008;177:1207-14 – Editorial: 1177-78). Many clinicians expect to provide relief targeting the inflammatory component of COPD. This may be the result of a misunderstanding of symptoms but it may also be linked to the relevance of exacerbations (for patients and physicians).

The details of the biology of COPD is still under research. Particularly, the inflammatory signal is mostly seen during exacerbations. In the meantime we, patients and physicians, are forgetting the stable presentation and probably the masquerading of this disease.

Inflammation as exacerbation or viceversa

COPD is not a disease of exacerbations only. COPD is a disease that exists when exacerbations are in their way. Not treating the stable component (chronic obstruction) will lead to an increase in the incidence of exacerbations.

However, the question is: what are the inflammatory markers of the disease if not the exacerbations?

Indicators of active disease

As it is indicated by Sin and cols. inflammation has its role in the progression of the disease. Inflammation also results in the systemic manifestations associated to the disease like muscle weakness, arrythmias, myocardial infarction, strokes, and sudden deaths (among several others). Of course, neither physicians nor patients want to wait for those indicators to be sure that there’s inflammtion to treat. We rely on the occurrence of exacerbations and, addressed by this, try to treat them although they don’t occur.

Chemical naturally occurring compounds

Some chemical substances have been associated to the development or progression of the inflammation in COPD. C-reactive protein, IL-6 and surfactant protein D (SP-D) are being considered markers of some good quality to assess the intensity of inflammation in the COPD patient. A measurement of this natural occuring substances may help support the occurrence of inflammation. Dr. Sin found that our prefered Trojan Horse for asthma have no impact on some of these components (CRP or IL-6) in patients with stable COPD. They did find a ralation with SP-D which synthesis is predominantly found in the lungs (assessed by mRNA expression).

Some questions

What is interesting from the published trial is that deficits in SP-D in mice results in development of emphysema (one on the manifestations of COPD). Then, why are we trying to reduce their elevated levels in COPD? Shouldn’t we try to encourage their increase?

Many questions may arise from the published results. Maybe SP-D is not the best biomarker in COPD neither (at least to follow therapy response). COPD has been getting increased attention of pulmonologists and other especialists. Thanks to this a new chapter in the medicine’s history is being written.

Diagnosis COPD based on exacerbations only?

The true is that we shouldn’t base COPD diagnosis on exacerbations. COPD diagnosis is based on the clinical record and a confirmatory spirometry. The biomarker of inflammation is still around by and it isn’t the clinical issue of exacerbations.

Asthma field is also hiding the “real” biomarker (an this disease has received attention). The point is that we know that the insult at the lungs develop a response and while in asthma the main response toward the end is inflammation in COPD it is chronic constriction.

Let’s talk and then treat

Patients need to talk about the differences between COPD and asthma to receive from them a good support in the diagnosis process. The patient may be the real biomarker (metaphorically), then we could first evaluate them and measure their whole response.