|
|
Chronic
Obstructive Pulmonary Disease |
| |
|
Overview |
|
|
Definition |
|
Chronic obstructive pulmonary disease (COPD) refers to a clinical syndrome of
chronic dyspnea as a result of expiratory airflow obstruction due to chronic
bronchitis or emphysema (often both). Chronic bronchitis is defined clinically
and is associated with chronic cough, resulting from excessive tracheobronchial
mucus production and impaired mucus elimination, lasting for at least three
months of the year for more than two consecutive years. Emphysema is defined
anatomically and is characterized by enlarged air spaces distal to the terminal
bronchioles with destruction of the alveolar walls; there is also a loss of
elastic recoil in the lung. In the United States, COPD affects an estimated 15
million people and is the fifth leading cause of death. |

|
|
Etiology |
|
- Smoking is the number one cause of COPD. Obstruction of airflow in
the small airways has been shown to be the earliest detrimental effect of
smoking.
- Exposure to environmental air pollutants
- Alpha1-antitrypsin deficiency, the only known inherited form of the
disease
|

|
|
Risk Factors |
|
- History of smoking or passive smoke exposure
- History of working with high levels of airborne particulates (e.g.,
dusts), gases, and fumes (such as coal and gold miners; farmers; and cement,
cadmium, and cotton workers)
- Low socioeconomic status
- Male gender
- Allergy and airway hyper-responsiveness (e.g., asthma)
- Women in undeveloped countries exposed to open fires for cooking and
heating
- Living in heavily industrialized urban areas
- Recurrent respiratory illnesses
- Family history of chronic bronchitis and emphysema (e.g.,
alpha1-antitrypsin deficiency)
- Emotional stress and repressed emotions have also been shown to
contribute
|

|
|
Signs and Symptoms |
|
Patients with emphysema present with a long history of dyspnea on exertion.
Patients with chronic bronchitis present with chronic cough productive of
sputum.
- Cough
- Cyanosis
- Weight gain
- Dyspnea on exertion (and eventually at rest)
- Excessive sputum production
- Wheezing
- Recurrent bronchial infections
- Weight loss in late stages
- Peripheral edema secondary to cor
pulmonale
|

|
|
Differential
Diagnosis |
|
- Asthma
- Bronchiolitis obliterans
- Pneumonia
- Lung cancer
- Cystic fibrosis
- Congestive heart failure
- Interstitial lung disease
- Primary pulmonary hypertension
- Acute viral infection
|

|
|
Diagnosis |
|
|
Physical Examination |
|
There is considerable variability in the clinical presentation of COPD, which
can range from simple chronic bronchitis (cough without airway obstruction) to
severe respiratory disability and fatal respiratory failure. The classic patient
with emphysema is often very thin and barrel chested and shows obvious
difficulty breathing, manifesting tachypnea (rapid respirations) with prolonged
expiration through pursed lips. Patients often assume a "tripod" position,
leaning forward while sitting, bracing with the arms. Cyanosis is not present so
the patient is considered a "pink puffer." The classic patient with bronchitis
is often overweight, even obese, and appears cyanotic. The respiratory rate is
normal, and there is no obvious distress. These patients are called
"blue bloaters." In reality most patients with COPD have a combination of
chronic bronchitis and emphysema. |

|
|
Laboratory Tests |
|
Show moderate to severe hypoxia |

|
|
Pathology/Pathophysiology |
|
In bronchitis:
- Hyperplastic and hypertrophied mucous glands in the submucosa of
large bronchi
- Increased Reid index (ratio of bronchial gland thickness to bronchial
wall thickness)
- Small airways: mucus plugging, goblet-cell metaplasia, airway
thickening, peribronchial fibrosis, mucosal and submucosal inflammatory changes,
increased smooth muscle, and accumulation of macrophages and neutrophils in
respiratory bronchioles
- Large airways: mucous gland enlargement, goblet-cell hyperplasia, and
squamous metaplasia
In emphysema:
- Enlargement of air spaces distal to the nonrespiratory
bronchioles
- Destruction of the alveolar
walls
|

|
|
Imaging |
|
- Chest X ray may show hyperinflation (flattened diaphragm, increased
retrosternal air space, outwardly bowed lower ribs), bulbous or cystic change,
especially in upper lung, and wide pulmonary diameter (due to pulmonary
hypertension).
- High-resolution CT can show areas of anatomic emphysema,
bronchiectasis, and allow measurement of pulmonary artery diameter.
- Echocardiography (two-dimensional, M-mode, or transesophageal) may
show characteristic changes of cor pulmonale, right atrial and ventricular
hypertrophy, and tricuspid regurgitation. It may allow estimation of the
severity of pulmonary hypertension.
|

|
|
Other Diagnostic
Procedures |
|
- Pulmonary function tests define the physiologic abnormalities of
COPD. Spirometry before and after bronchodilator administration confirms airflow
obstruction and helps in assessing the severity and reversibility of lung
damage. Lung volume measurements (e.g., plethysmography) show characteristic
overinflation. Diffusion capacity is impaired in COPD.
- Arterial blood gases may show hypoxemia, hypercapnea, or
both.
- Exercise testing (i.e., on a treadmill or stationary bicycle, 6- or
12-minute tests) will show reduced exercise tolerance and exercise-induced
hypoxemia.
|

|
|
Treatment Options |
|
|
Treatment Strategy |
|
Smoking cessation is the key to preventing exacerbations and progression.
Management is dependent on the degree of obstruction, the severity of
disability, and reversibility of the illness. Respiratory infections must be
treated aggressively. |

|
|
Drug Therapies |
|
- Alpha1-antitrypsin replacement therapy
- Supplemental oxygen (1 to 3
liters/min)—dosage should be appropriate to relieve
hypoxemia (i.e., to maintain a PaO2 of 55 to 60 mm Hg)
- Bronchodilators—to increase airflow and
reduce dyspnea
- Anticholinergic agents (e.g., ipratropium, 0.18 mg, 2 puffs
qid)
- Beta2-adrenergic agonists (e.g., metaproterenol,
terbutaline, or albuterol, 2 to 6 puffs every three to six hours)
- Theophylline (200 to 400 mg bid)—requires
frequent blood monitoring for toxicity
- Corticosteroids (e.g., prednisone, 40 mg/day for two weeks then
reduce to 0 to 10 mg every day or on alternate days)
- Broad-spectrum antibiotics (e.g., ampicillin or amoxicillin, 2 g/day;
erythromycin, 2 g/day; or trimethoprim-sulfamethoxazole, 1 double-strength
capsule/day)—for treatment of exacerbations
- N-acetylcysteine—for mucolytic therapy;
however, it may cause bronchospasm
- Magnesium can also be markedly helpful as an IV infusion of 5 to 10 g
of elemental magnesium over 6 to 10
hours.
|

|
|
Complementary and Alternative
Therapies |
|
May be very helpful at decreasing the symptoms and preventing infections.
Since smoking cessation is very important, the alternative treatments for this
will be listed. Psychotherapy and support groups can be very helpful in learning
to cope with chronic disease. |

|
|
Nutrition |
|
- Dairy products and bananas increase mucus buildup and should be
avoided. Garlic, onions, and horseradish may actually decrease mucus production.
IgG ELISA food allergy testing can determine other foods that can cause
inflammation in the lungs.
- Some essential fatty acids are anti-inflammatory, dose is 1,000 to
2,000 IU, mixed omega-3 and omega-6 oils (flaxseed, fish, borage, and/or evening
primrose oil; avoid vegetable oils and saturated fats)
- Coenzyme Q10 prevents fatty acid oxidation and increases exercise
tolerance as a cardio-protective antioxidant. Dose is 10 to 50 mg
tid.
- Other important antioxidants: selenium (200 mcg/day), vitamin E (400
IU/day), vitamin C (1,000 mg tid), L-carnitine (750 mg bid). Note that
beta-carotene increases the risk of lung cancer in smokers.
- Bromelain is a mucolytic, 250 to 500 mg tid away from meals. People
with pineapple allergy may be sensitive to this product. Bromelain may also
aggravate gastritis.
- N-acetylcysteine is a mucolytic, 400 mg tid.
- Magnesium promotes muscle relaxation in bronchial smooth muscle and
blood vessels (100 to 500 mg bid). Magnesium may cause diarrhea in some
sensitive individuals.
|

|
|
Herbs |
|
Herbs are generally a safe way to strengthen and tone the body's systems. As
with any therapy, it is important to ascertain a diagnosis before pursuing
treatment. Herbs may be used as dried extracts (capsules, powders, teas),
glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless
otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water.
Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for
roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as
noted.
- Mullein (Verbascum densiflorum): expectorant, soothes
irritation
- Ginger (Zingiber officinale): dissolves secretions, relieves
bronchial spasms
- Fennel (Foeniculum vulgare): dissolves secretions, mild
antispasmodic, calming digestive stimulant
- Coltsfoot (Tussilago farfara): anticatarrh, demulcent.
Prolonged use may cause liver damage due to pyrrolizidine alkaloids.
- Licorice (Glycyrrhiza glabra): antiviral, antidepressant,
soothing, anticatarrh, contraindicated in hypertension
- Hawthorn (Crataegus monogyna): protective of blood vessels,
increases cardiac output without increasing cardiac load
Mix equal parts of herb, or tincture of four to six of the above herbs. Dose
is 1 cup tea tid, or 30 to 60 drops tincture tid.
Essential oils: eucalyptus (Eucalyptus globulus), thyme (Thymus
vulgaris), rosemary (Rosmarinus officinalis), and/or lavender
(Lavandula angustifolia): place 3 to 5 drops in 2 cups of water in a
humidifier to prevent infection. |

|
|
Homeopathy |
|
Constitutional treatment by a homeopathic prescriber may help with symptoms
and address underlying emotional issues that will aid patients in smoking
cessation. |

|
|
Physical Medicine |
|
- Castor oil pack: Used externally, castor oil is a powerful
anti-inflammatory. Apply oil directly to skin, cover with a clean soft cloth
(e.g., flannel) and plastic wrap. Place a heat source (hot water bottle or
heating pad) over the pack and let sit for 30 to 60 minutes. For best results
use three consecutive days in one week. When placed over the lungs, castor oil
packs decrease inflammation and stimulate drainage.
- Postural drainage, yogic breathing, and pulmonary rehabilitation
programs may all be helpful.
|

|
|
Acupuncture |
|
Has been shown to have great benefit in smoking
cessation. |

|
|
Patient Monitoring |
|
Serial monitoring of pulmonary function is performed annually or as symptoms
dictate. If patient is unstable or if home oxygen is required, more frequent
visits are needed. |

|
|
Other
Considerations |
|
|
Prevention |
|
Cessation of smoking is the single best way to prevent disease progression.
Respirators of the appropriate type can reduce the risk to workers exposed to
dusts, fumes, and gases.
Negative air ion generators are frequently helpful. Electronic air cleaners
and HEPA filters are helpful in highly polluted environments and for persons who
have a marked allergic basis for their chronic bronchitis contribution to
COPD. |

|
|
Complications/Sequelae |
|
The most common complication of COPD is pulmonary infection. Prophylactic
influenza vaccination (annually) and pneumococcal vaccination (every six to
eight years) can be effective. Patients on steroid therapy are at risk for
steroid-related complications—adrenal suppression,
capillary fragility, easy bruisability, glucose intolerance, weight gain in the
face, and muscle wasting. |

|
|
Prognosis |
|
By the time dyspnea develops with simple daily activity, patients may have
lost two-thirds of their pulmonary function. The diagnosis is often made very
late in the course of the disease. Thus, the mortality rate after diagnosis is
high (>50% after 10 years). |

|
|
Pregnancy |
|
With the exception of patients with alpha1-antitrypsin deficiency,
women are usually diagnosed with COPD well beyond the reproductive
years. |

|
|
References |
|
Blumenthal M, ed. The Complete German Commission E Monographs: Therapeutic
Guide to Herbal Medicines. Boston, Mass: Integrative Medicine
Communications; 1998:423, 468.
Bordow RA, Moser KM. Manual of Clinical Problems in Pulmonary
Medicine. 4th ed. Boston, Mass: Little, Brown; 1996:212-215.
Celli BR. Pulmonary rehabilitation in patients with COPD. Am J Respir Crit
Care Med. 1995;152:861-864.
Duke JA. The Green Pharmacy. Emmaus, Pa: Rodale Press; 1997:93-95,
179-183.
Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles
of Internal Medicine. 14th ed. New York, NY: McGraw-Hill;
1998:1451-1457.
Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary
disease. N Engl J Med. 1993;328:1017-1022.
Snider GL. Standards for the Diagnosis and Care of Patients with Chronic
Obstructive Pulmonary Disease. Washington Crossing, Pa: Scientific
Frontiers; l996:1-12.
Woodley M, Whelan A. Manual of Medical Therapeutics. 27th ed. Boston,
Mass: Little, Brown;
1992:200-202. |

|
Copyright © 2000 Integrative Medicine
Communications This publication contains
information relating to general principles
of medical care that should not in any event be construed as specific
instructions for individual patients. The publisher does not accept any
responsibility for the accuracy of the information or the consequences arising
from the application, use, or misuse of any of the information contained herein,
including any injury and/or damage to any person or property as a matter of
product liability, negligence, or otherwise. No warranty, expressed or implied,
is made in regard to the contents of this material. No claims or endorsements
are made for any drugs or compounds currently marketed or in investigative use.
The reader is advised to check product information (including package inserts)
for changes and new information regarding dosage, precautions, warnings,
interactions, and contraindications before administering any drug, herb, or
supplement discussed herein. | |