Definition and Determinitaion

Asthma is narrowing of the lungs caused by muscle tightening and clogging of the airways by inflammation. This can be caused by exposure to pollens, animals, cigarette smoke and pollution. Asthma is diagnosed when a patient is determined to have a reversible airway obstruction after using a bronchodilator such as albuterol. Patients are measured against a standard curve for height weight and sex. Also, some adjustment is made for African-American body types, with the normal values multiplied by eighty-five percent. After an initial testing, the patient inhales a bronchodilator and waits twenty minutes. If lung function has improved twelve percent, the patient is considered to have reversible airway disease, or asthma.

However, asthma is also evaluated by how patients report feeling. A well-conditioned athlete can "fool" the pulmonary function test and do better than eighty percent even though they may have severe asthma symptoms and wheezing on physical exam.

Medication is the mainstay of asthma management. Various medications can treat allergic conjunctivitis and allergic rhinitis, including antihistamines, anitleukotrienes, nasal steroids and nasal antihistamines for nasal congestion. Oral antihistamines, ocular antihistamines and mast cell stabilizers can treat the ocular and throat symptoms.

The first step is to avoid asthmatic triggers. This includes keeping pets out the bedroom, removing carpet and rugs, using dust mite covers on the beds and installing HEPA filters to keep down the level of pet dander. Patients should avoid going out of doors in the morning between 6 a.m. and 9 a.m., when pollen levels are at their highest. Patients should be tested to determine their sensitivity to pollens, dust mites, dog and cat dander and cockroaches. Immunotherapy or allergy desensitization is indicated for patients to decrease their sensitivity to the allergens that trigger their asthma. Sixty percent of asthmatics are allergic to some antigen, and triggers by immunotherapy can significantly decrease the amount of medication needed for their asthma. If, after treatment and repeated doses of prednisone, the patient continues to have flares of asthma, the patient is a candidate for Xolair, a monoclonal antibody that wipes out IgE.

Triggers

Asthma is a disease that can have variable outcomes and variable measures of severity. Typically, patients underestimate the dimension and severity of their symptoms, and can spend months coughing, wheezing and experiencing shortness of breath, without realizing how severe the underlying disease is. Half of all asthmatics are unable to accurately estimate the degree of the asthma, and less than 30% comply with their prescribed medical regimen.

One way to determine the subjective feelings of the patients is the ACT (Asthma Control Test), a questionnaire validated by medical studies. The ACT presents five questions and assigns one of five point scores to them. The nature of the questions – e.g., how many times a patient is waking up at night – help measure the severity of the case in a way that objective methods sometimes miss. A patient with a score of nineteen or higher in an ACT is considered well-controlled.

Objective measures such as pulmonary function tests can measure the amount of obstruction and reversibility of airway disease. The peak flow meter – a hand-held device used to measure how air flows from a patient’s lungs - was invented to fulfill this need. Based on three maximum exhalations, the strongest measure is taken and compared to a normal value for those of the patient’s height and weight. The variability between the nighttime and daytime measure is also taken into account. An average unstable asthmatic can have his or her peak flow vary by up to fifteen percent between nighttime and daytime, as opposed to less than five percent for a normal stable non-asthmatic. This is due to changes in hormonal patterns and exposure to allergens at night among many other factors.

Recently, nitrous oxide has been used to measure the level of inflammation in asthmatics. With the use of special censors, the patient’s level of inflammation can be determined with a thirty-second breathing pattern. However there is controversy as to the absolute level of nitrous oxide that separates asthmatics from non-asthmatics.

There is a difference of opinion in how much weight to give to each measure of severity of the asthma. Most drug studies that measure the efficacy of asthmatic drugs use FEV 1 or how much air is blown out in one second as the most reproducible measure of asthma severity and reproducibility. Finally measures need to be used to convince the patient of the severity of their asthma so that they will comply with their prescribed medical regimen.

Preventative Measures

Allergic rhinitis is an inflammatory response of the nasal passages to pollens that happens through an IgE mechanism. Visually, IgE molecules are like two telephone poles strung on a mast cell. These molecules release chemicals – including histamine, bradykinins and leukotrienes – when they connect to a pollen particle, which causes allergic symptoms

However, allergic rhinitis of the upper airways and a smoking history can be confounding variables. Nitric oxide can are produced by both the upper airway and lower airway and therefore can not distinguish upper airway inflammation from lower airway inflammation. Smokers must quit four to eight weeks before being measured or the smoking will lead to higher levels above twenty.

Vasomotor rhinitis is synonymous with non-allergic rhinitis. The patient does not make antibodies against pollen as a cause of the nasal inflammation. Instead changes in temperature, humidity, odors or a broken or surgically repaired nasal septum may predispose to nasal stuffiness.

Pollens tend to pollinate between the hours of 6 a.m. and 10 a.m. Any medication must be directed towards those hours. In the spring in the northeast tree pollens usually arrive in March and last until mid-May. Grass pollens are most prominent from mid-May until mid-July; ragweed pollen, in September. Mold pollen occurs throughout the year. Dust mites also occur throughout the year when humidity exceeds forty percent.

Prolonged exposure to indoor pets such as cats or dogs can lead to symptoms that last all year round. Pets usually leave excessive dander in the bedroom Patients sleep in the bedroom for eight hours a night and are exposed to pet dander at one hundred times the amount of exposure to pollens which my only last for six weeks. Also, New York City apartments tend to be one-third the size of normal houses, giving dander less places to hide.

Cats secrete dander that is five microns in diameter and they can go five generations or very deep into the lungs. Dog dander is twenty microns in diameter and doesn’t go as deep into the lungs. Cat dander can stay airborne for five hours, as opposed to twenty minutes for dog dander and dust mites. Therefore there are more patients allergic to cats than dogs.

A patient may experience a severe nasal drip during September or March, which will often get attributed to allergies by the sufferer. However these are the times of the year when changes of temperature and rain are most prevalent in the atmosphere. The only way to distinguish the difference between allergic and non-allergic rhinitis is with allergy skin testing for immediate diagnosis, or an ImmunoCAP blood test for results in 4-5 days. The patients typically do well with a combination of a nasal steroid and a nasal antihistamine spray.

Environmental controls can be done to decrease the pet and dust mite exposure. Use of dust mite covers on the bedding, and taking the carpet up in the bedroom, can decrease the presence of dust mites. Dust mite covers must be washed above 140 degrees to be effective. Use of Allerpet and air filters can significantly decrease pet dander in the bedroom. However, an air filter is ineffective against dust mites, as they are larger than cat dander and usually settle on surfaces, without staying airborne long enough to be filtered by a machine.

Air conditioning is the best treatment for filtering early morning pollination. Complications of nasal allergies can include acute or chronic sinusitis, acute sinusitis and bronchial asthma. These diseases are indications for immunotherapy which can prevent the development of these conditions.

Medication and Implications

Nitric oxide is a biomarker for inflammatory mediators that reflect activity of the eosinophils, which are the main marker for severity of inflammation in asthma. The definitive test is a BAL (bronchialalveolar lavage) of eosinophils, which correlates with effectiveness of inhaled steroids. FeNO (fractional exhaled nitric oxide) can now be measured by portable devices such as the mini portable meter or the aperion device. Levels above 20 parts per billion are correlated with non-control of asthma.

Recently, nitrous oxide has been used to measure the level of inflammation in asthmatics. With the use of special censors, the patient’s level of inflammation can be determined with a thirty-second breathing pattern. However there is controversy as to the absolute level of nitrous oxide that separates asthmatics from non-asthmatics.

Inhaled steroids control the inflammation and deliver the drug to the site of the disease without a large amount of systemic absorption. Some common prescriptions include mometasone, fluticasone, beclomethasone, budesonide and combination therapy of Serevent, fluticasone, foradil and budesonide. The drug combinations are generally for more severe asthma. Also albuterol and other short-acting inhalers act as rescue medication, which patients use to reverse an immediate feeling of short breath. The chlorofluorocarbon previously used in these inhalers has been replaced with hydrofluoroalkane, to decrease the effect on the ozone layer.

The doses, given in micrograms (unlike an oral does, which are typically administered in milligrams) go to all parts of the body, and can create many side effects. Drug allergy can involve many different compounds and types of reactions, but the two most common culprits are penicillin and sulfur drugs. Penicillin is the most common form of drug allergy over the last 65 years. The major antigen is the six carbon benzene ring that people react to. Patients usually develop a maculopapular rash, a diffuse red rash on the body or centripetal rash, which spreads out to the legs and arms.

Currently, there is no adequate test for penicillin allergy. One needs to test with both penicilloyl-polylysine or PPL to test the major determinants, and an MDM (minor determinant mixture) to check for fatal reactions. As the penicillin passes through the liver it is hydroxylated, sulfated and combines with albumin to produce different chemical compounds. The fatal reaction usually happens to the MDM. If necessary, one must do a graded penicillin challenge if the patient has a history of reacting to penicillin. However there has never been a fatal reaction to penicillin through the oral route.

Sulfur is the second most common drug allergy in general medicine. Sulfur is present in water pills, celecoxib, Bactrim and Azulfidine anti-arthritic drugs. Because the liver is often a slow hydrolyzer, some patients digest sulfur slowly, resulting in the body being exposed to the chemical for longer periods of time. The most common manifestation of an IgE allergy to sulfur is a maculopapular rash. The patient can develop Stevens-Johnson Syndrome, or ulcers to mucosal surfaces such as the vagina, anus or mouth. This type of lesion can become a toxic epidermal necrolysis or a virtual burn. Patients can be desensitized to IgE sulfur reactions, but not Stevens-Johnson Syndrome.

Sulfur drugs can also absorb sunlight and cause a photosensitive reaction on the sun exposed surfaces. These typically appear on the face, and the tops of the hands and feet. Finally most drugs – even if they don’t cause IgE reactions – can be inured against when the need for a life saving therapy outweighs the patient’s history of an allergic reaction. A patient can be administered one hundredth to one thousandth of the dose, which is then doubled every half hour until the patient gets a therapeutic amount. A rush desensitization can be can be done in one day, and a slow one can be broken down to take one month.

In addition nasal saline with several companies such as ENTSOL and Neilmed provide a wash that is capable of restoring the nasal cilia. It helps the hairs in the nose to continue to dispose of the mucous in a coordinated way. However there is no permanent remediation for this condition. Finally patients can get rebound symptoms from overuse of afrin or other vasoconstrictors. This can lead to a permanent nasal congestion although use for five days or less does not usually cause congestion.

Finally the patient should be given a regimented treatment plan to indicate when they should step up their medication if their peak flow falls by ten percent or more. All of these measures may need to be taken into consideration when deciding how much medication to put an asthmatic on and much medication to decrease when the patient is not in the peak asthmatic season. All of these measures are incorporated into the new asthma guidelines published by the National Institute of Health to judge the severity of asthma.