DISCLAIMER
The information contained in this site is intended to
help individuals who have or think they may have allergies and/or asthma. This information is intended to increase your
understanding of allergies and asthma. The
information presented is not to be used to make a diagnosis or form any
treatment plan. Both diagnosis and
treatment must be based on a complete history, a thorough physical exam, and
appropriate skin, laboratory, and pulmonary testing done under the direction of
a physician with experience in this area.
Dr. Sweet assumes no responsibility for any misuse of this information
including but not limited to any loss or injury.
WHY
After clearly
stating I am not responsible for any problems resulting from the information in
this web site, why on earth would I bother to spend my time producing it? I have been on the internet for years and try
to read every article and journal possible on both allergies and asthma. The variety of sites available range from
very scientific, peer reviewed and reliable (but unfortunately often very
difficult for the average person to understand) to personal sites which are
highly emotional, unreliable and dangerous to your health. This site represents an attempt to fill the void
between these two extremes. It reflects
up to date medical research but also represents my own experience and personal
opinions. The materials are presented in
much the same way that I discuss allergies-asthma with my patients and
represents an attempt to make this clearly understandable to the individual
with allergies-asthma. Please feel free
to download or print any of this information.
WHO AM I
It's very
important that the reader understand not only my medical qualifications but
have an appreciation of how I approach allergic problems. When I was in my teens, I developed severe hayfever (ragweed) that literally almost killed me. My life was turned around by an allergist and
immunotherapy (allergy shots). I was an
allergy patient long before I was a M.D.
I graduated from university in Applied Science (engineering) and became
a Professional Engineer working in the nuclear power industry, then
subsequently retired from engineering (P.Eng.r) and
decided to go into medicine. I graduated
from medical school in 1976 and began a general practice in northwestern
THE ALLERGIC PROCESS
When the body
contacts a foreign substance (inhaled, ingested, direct contact, etc.) certain
cells in the immune system of the body identify this substance and produce
antibodies that can specifically identify and neutralize this foreign
substance. An example of this would be a
bacterial infection causing a sore throat, the immune system produces
antibodies against this specific bacteria, the infection is cleared, and the
immune system settles back to normal. We
normally produce several different antibodies that have specific purposes: IgA,
IgG, IgM, and IgE. We are interested in
the IgE antibody. IgE is normally
produced to fight parasitic infections.
The TH2 lymphocyte is responsible for controlling and encouraging the
production of IgE. The TH1 lymphocyte
acts to balance the immune system and prevent over production of IgE. In individuals with allergy the TH2
lymphocyte predominates which leads to an overzealous IgE response to
substances such as dust mite allergen, pet allergen, pollens, mold spores,
foods and drugs. It takes several days
for the immune system to identify and produce a specific IgE antibody to a
specific substance (i.e. penicillin).
This is important, as you cannot have IgE antibodies to a specific
substance unless you have had previous prior exposure or have been exposed for
several days to allow the body to produce IgE.
The IgE antibody is attached to the surface of certain cells (mast
cells, basophils). The mast cell contains
many small internal packages filled with chemicals. When IgE antibodies on the
surface of the mast subsequently (on reexposure)
identify the specific penicillin molecule, the mast cell immediately releases
all its contained chemicals into the surrounding tissues. These chemicals cause swelling and irritation
in the affected tissues. This is known
as the acute or early phase reaction and is responsible for the immediate
allergy symptoms seen when an individual who is cat allergic gets close to a
cat (the eyes, nose, chest often are affected, because these tissues contain
many mast cells, if the cat licks the skin you get a hive because the skin
contains many mast cells) and this reaction is responsible for anaphylaxis
(i.e. a severe penicillin or peanut allergy causes the mast cells in many
different areas (skin, respiratory, heart, gut) to release all their chemicals
at once). However, some of these
released chemicals don't cause immediate symptoms, but do attract other cells
to the site of the allergic reaction.
These cells take approximately six hours to arrive, and once they are at
the site of the allergic reaction, cause further swelling and irritation
(inflammation) that can last for many hours to many days. A cell that we are particularly interesting
in is the eosinophil, which is linked with IgE production, and can cause long-term
inflammation in the tissues. This late
inflammatory response caused by the eosinophil (and some other cells) is called
the late phase or delayed allergic reaction and is responsible for the ongoing
& continuous symptoms seen in chronic nose and sinus problems, and
asthma. Asthma is interesting, because
once the inflammatory process is started, it tends to keep going on its
own. This occurs in individuals with
chronic nasal allergy.This late phase reaction is
also responsible for the secondary allergic reaction you occasionally see in
anaphylaxis 6 to 12 hours after the initial reaction occurred.
So now you have a basic understanding of the allergic reaction. This reaction is caused by an over active
response of the immune system, driven by TH2 lymphocytes, producing excess IgE
to substances we normally don't, the IgE is highly substance specific, requires
reexposure or prolonged exposure, this exposure
results in a release of chemicals from the mast cell that results in an
immediate, acute, early phase reaction and a secondary delayed late phase
reaction produced by cells moving to and staying at the allergy site
(particularly eosinophils) causing prolonged inflammation. This type of
allergic reaction is termed type 1, immediate, IgE mediated. There are other types of allergic
immunologically mediated reactions, types 2, 3, and 4 and they will be
mentioned later on when discussing specific allergy problems. What is critical, is that you realize the
allergic reaction causes inflammation.
There are reactions that cause mast cells to release their chemicals
that are not mediated by the immune system (i.e. ASA can cause mast cells to
directly release chemicals). It is
important to know whether a reaction is truly allergic (caused by IgE and the
immune system) because we have good medications available to treat many true
allergic reactions and allergy skin testing only confirms IgE reactions. You
should also realize that the allergic response is an over aggressive immune
system response (not a form of immune system weakness). Perhaps an analogy will help. The immune system is like a huge orchestra,
made up of many different players (cells) each producing there own sounds
(chemicals). Normally all you see or
hear is the total visual effect and sound of the orchestra-the normal immune
response. However, specific members of
the orchestra can do solo performances (while the rest of the orchestra is
still playing) and in the allergic orchestra the conductor is the TH2
lymphocyte, a common sound heard is IgE
antibody, and the mast cell does a solo performance in the immediate (acute)
allergic reaction (examples would be anaphylaxis or the acute nasal/eye
reaction on exposure to a substance one is allergic to (allergen)), while the
eosinophil does a solo performance in the late phase (delayed, chronic)
allergic reaction (examples would be chronic allergic rhinitis, asthma).
THE PROBLEM
Allergies and
asthma are increasing at a staggering rate.
Estimates for most western countries are that allergies and asthma have
doubled in the adult population within the last 10 to 15 years, and likely
tripled in young children in the same time span. No other common disease process has increased
so radically in modern times. Estimates
are that asthma alone is occurring in up to one in ten adults and possibly as
high as one in five children in western countries. This massive increase can only be caused by
our environment (in the broadest sense) because our gene pool does not change
this rapidly. Another way of looking at
the problem is why are individuals developing a primary TH2 lymphocyte response
(remember this response increases IgE, allergies, asthma). Many theories have been put forward, but
these are mostly from epidemiologic-statistical studies that cannot precisely
prove a causal relationship. Some of
these theories include: smaller family size, sibling order, immunizations,
frequent antibiotic use, reduced number of specific infections (? bowel
infections), various pollutants, smoking
during pregnancy, the striking increase in dust mite (cockroach in inner
cities) allergens due to modern energy efficient carpeted housing, etc.. The “hygene
hypothesis” is gaining popularity where a general reduction in childhood
infections and reduction in exposure to certain markers of infection
(endotoxin, etc.) allow the immune system to slide toward the TH2
response. The answer to this question
will likely be multifactorial and difficult to solve with one or two specific
interventions. We are sure, however,
that this increase is truly occurring.
How we can reduce the TH2 response (or conversely increase the TH1
response) will be difficult to attain if we don't know the causes in the first
place.
RESPIRATORY ALLERGY & ASTHMA
OVERVIEW
It is important
to have a broad understanding of the respiratory system to appreciate the
allergic problems that arise. The lining
of the respiratory tract is fairly similar throughout. It is designed to pick
up small particles on its surface mucus and then move this thin layer of mucus
and particles back out the respiratory system (usually to be swallowed). The
lining also functions to warm and humidify the air - particularly the
nose. When particles of a substance that
one is allergic to land on the respiratory lining you develop allergic
inflammation in and under the lining.
This inflammation causes swelling of the lining, excess mucus secretion,
and nerve irritation. Individuals will
often have one symptom that will predominate at any given time and this
frequently changes over time. In the
nose you get a plugged-stuffy nose, a runny nose, and sneezing. In the sinuses
you get swelling-pressure, mucus production (post nasal drip), and
pressure-pain-nausea. Swelling of the sinus openings leads to mucus retention
and possible secondary infection of the retained mucus. If the lining of the
nose is inflammed at the back and side of the nose,
the eustachian tube starts here and runs up to the
middle ear (the pressure equalizing tube for the middle ear) and involvement of
this area results in recurrent ear problems, particularly in infants and small
children. If the allergic process involves the larynx (voice box) you develop
allergic laryngitis - your voice changes pitch or you lose your voice. If the allergic process goes further down to
involve the trachea (the large single air tube in the center of the chest) all
you usually get is a cough, occasionally with slight mucus and central chest
discomfort, but never any shortness of breath.
Continuing down the respiratory tract you get to the medium and small
tubes of the lungs where the inflammatory allergic process causes swelling,
mucus production, nerve irritation (cough), and the tubes become overly
sensitive to a variety of allergens, stimuli and irritants and can narrow down
causing wheezing or shortness of breath (asthma). Similar to the sinuses, allergic inflammation
sets up increased possibility of infection in the middle ear and lungs. What is important, is that the entire
respiratory tract is a continuum and it is very common for more than one area
to be involved at the same time with the allergic inflammatory process. It is not unusual for the allergic process to
skip areas also (i.e. there may be signs of mild allergic nasal problems and
asthma) with no evidence of any problems in between. This is dependent upon the specific allergy
particle, it's size, shape, aerodynamics, the type of
breathing (mouth, nose, both), and a host of factors we likely don't
understand. An important principle, is
that allergic inflammation (or infection) in the upper airway can adversely
affect the lower airways and make asthma worse (the converse of this is also
true, that controlling upper airway allergic inflammation improves asthma
control).
SPECIFIC SYMPTOMS
Little time
will be spent on the standard symptoms that most individuals know. A few comments are important. It is very difficult at times to tell the
difference between allergic nasal problems and a typical cold-viral
infection. Most viral upper respiratory
infections start in the nose and track into the chest in approximately 48
hours. Most have gone within 10
days. If you have generalized aching and
a low grade fever at the start it is likely viral. Any significant fever makes the diagnosis of
infection. Allergy symptoms often last
longer, and any "cold" lasting longer than 2 weeks is highly
suspicious of allergy. Any cold, cough,
or respiratory symptom that returns seasonally is allergic until proven
otherwise. Sneezing usually represents
allergy, particularly if it lasts more than a few days, and definitely if
specific exposures trigger the sneezing.
Post nasal drip comes mainly from the sinuses, goes down the back of the
throat, often is very tenacious and thick, and individuals with this problem
frequently clear their throat.
Cough has to be
discussed more thoroughly. The nerves
that trigger the cough reflex are found in the back of the throat and all the
way down the tubes in the lungs. There
are multiple causes of cough and it is not unusual for more than one cause to
be involved. Post nasal drip is a common
cause of cough. Allergic inflammation in
the large central tube of the airways (allergic tracheitis)
is often overlooked. It frequently is
seasonal and never causes significant difficulty breathing. Asthma-the smaller tubes involved-often
causes cough in association with mucus production, episodic wheezing or
difficulty breathing, and occasionally cough (particularly at night, or with
cold air exposure or exercise) is the only symptom (cough variant asthma). Infection is an extremely common cause of
cough and specific infections can cause coughing that lasts several weeks. Reflux-movement of acid from the stomach into
the esophagus (the tube you swallow food down)- can
irritate the nerves supplying the esophagus and result in coughing. Reflux also can make asthma worse. Up to one third of people with significant
reflux do not have any symptoms of heartburn.
After taking a careful history and doing a good physical exam, it's
often appropriate to treat what you feel the main cause of cough is, and if the
cough is eliminated, you have your diagnosis.
However, for individuals with chronic cough, further investigation and
elimination of one cause at a time is often required. Cough is often a huge problem for parents who
cannot sleep with their child coughing, yet the child often is relatively
unaffected, and severe fatigue can result from lack of sleep (see the
subsection on Cough). Chronic cough associated with other
constitutional symptoms (night sweats, weight loss) can indicate a serious
disease process. True wheezing usually
indicates asthma. The problem is that
many individuals do not know what "wheezing" is. This is a high pitched whistling sound that
comes from the chest itself. Wheezing
occurs when the smaller tubes in the lungs are narrowed significantly. This is not to be confused with stridor,
which is the sound made when the throat or larynx are severely swollen and it
is difficult to move air in and out.
Stridor sounds like someone is grabbing your neck and choking you.
ALLERGIC RHINITIS - THE NOSE
Allergic
inflammation in the nose occurs in 2 basic forms. Seasonal allergic rhinitis-hayfever-occurs during a specific season and is usually
caused by pollen or occasionally by seasonal molds. It is often accompanied with allergic eye
irritation-itching, tearing, pink to red color- allergic conjunctivitis. Perennial or chronic allergic rhinitis occurs
continuously throughout the year although it often is worse at certain
times. This is caused by chronic
exposure to year round allergens (dust mite, pets, molds)
or the individual has seasonal allergies for every season. Because the nose is the entrance to the
airway and acts as the main filter, many individuals with respiratory allergy start
with allergic rhinitis. Interestingly,
many individuals do not notice this problem, either accepting it as normal or
thinking they just have frequent or severe colds. Again, no infection ever comes at the same
time of year, repeatedly or usually lasts for more than ten days. Allergic rhinitis is often associated with
other respiratory allergy in the sinuses, ear, or chest.
There are
several other forms of rhinitis that you should be aware of. Irritant rhinitis, caused by many and varied
irritants is extremely common. Chemicals
of many kinds, smoke, solvents, cleaning agents, etc. can all cause chemical
irritation of the respiratory lining.
This is a direct chemical irritant effect. The treatment for irritant rhinitis is
avoidance of the irritant. Every
individual with allergic rhinitis is more sensitive to irritants than
non-allergic normal individuals. This is
an important concept. If you have pre
existing allergic inflammation of the respiratory lining, any chemical or
physical irritant will cause more severe symptoms than in a normal
individual. A simple analogy is
appropriate. If you have no allergies,
and take a cup of vinegar and pour it over your arm, nothing happens. If you have allergies, the skin on your arm
is inflammed by the allergic process, take sand paper
and rub the skin on your arm until it is raw and oozing, then pour vinegar on
the arm. This is what irritants do to
people with allergies. Vasomotor
rhinitis is also extremely common and can also occur with allergic rhinitis. Vasomotor rhinitis is typically a profuse
runny watery nose. The nasal discharge
is clear, and is usually triggered by changes in temperature, other physical
stimuli (such as CPAP for sleep apnea), eating hot or spicy food, etc. This type of rhinitis is caused by overactive
nerves that supply the mucus secreting glands in the nose.
Allergic
rhinitis often presents as a plugged or stuffy nose. Adults with allergic rhinitis often gradually
develop allergic sinusitis over a period of years. Only in recent years have we realized that
the most important inflammatory response in allergic rhinitis is the late phase
reaction driven by the eosinophil, which is why anti-inflammatory medication is
the single best treatment. When the nose is primarily stuffy in the major or
when getting up in the morning, it often signifies the individual is allergic
to allergens in the home. Seasonal
allergies can often be identified if the individual clearly knows exactly when
there nose flares. Nasal symptoms appearing
in the very early spring as the snow is melting or very late fall often
identifies mold allergy, symptoms occurring later in the spring as things turn
green and warm up often indicates tree pollen allergy, summer usually June-July
is associated with grass pollen allergy, and early fall (Aug.-Sept.) usually is
caused by weed pollen allergy. I am often quite surprised at how the
allergic seasonal patient is not clearly aware of exactly when their symptoms
occur. What is critical, is that any
suspected inhalant allergy must be confirmed by appropriate skin testing. There are also huge variations in the timing
of the appearance of specific allergens depending upon your geographic
location. This is why it is so important
to be allergy tested by an allergist in your specific area that knows the
details of the specific allergens in your area.
In my area,
Treatment of
allergic rhinitis is similar to the basics required to treat any allergic
condition. The primary treatment is
ALWAYS avoidance first of. When this is
applied to indoor allergens (dust mite, indoor molds, animal
allergen) avoidance measures can be extremely effective. However, avoidance of outdoor allergens is
more difficult (although they can be avoided indoors by keeping windows closed
(particularly the bedroom window), with central air conditioning, and using
medication is usually required. The
single best medication for allergic rhinitis is the topical nasal
anti-inflammatories (corticosteroid nasal sprays) which have been shown to be
superior to antihistamines and decongestants.
The topical anti-inflammatory nasal sprays are safe when used as
directed and are most effective when used regularly to decrease the allergic
inflammation and maintain the lining of the nose as close to normal as possible
(a similar situation exists in treating asthma). However, the addition of an antihistamine to
nasal anti-inflammatories gives an additive effect for many individuals and
represents the common medication combination used for allergic rhinitis. Please refer to the specific subsection on
Avoidance Measures, particularly the Dust/mold Free Bedroom, and to the specific
section on Medications, particularly the instruction sheet on how to use topical nasal sprays ( nobody, including
the manufacturers give correct instructions for the use of these sprays - please see my instruction sheet) and how to
use nasal saline solutions.
ALLERGIC SINUSITIS
The respiratory
lining continues with no interruption into the sinus cavities. Please see the details of the individual
sinuses in the anatomy section. Allergic sinusitis is extremely common in
association with allergic nasal problems and often develops in adults after a
number of years of pure nasal symptoms.
Allergic sinusitis is vastly under appreciated and under recognized by
the public and physicians alike ( as is the extremely
common allergic eustachian tube dysfunction - ear
problem). Also, the word sinus means a variety of things to different
individuals. Often when I take a family
history for allergy-with negative results, I will then ask if there have been
any sinus problems in the family, with a very common response that several
individuals in the family have " sinus
". Medically, sinusitis refers
specifically to inflammation in the sinus lining. The allergic inflammatory response can occur
in the sinus respiratory lining just as it can in the nose and chest. What is often not appreciated is that the
allergic process itself causes symptoms without infection being present. When the sinuses produce excessive mucus, the
majority of this mucus goes down the back of the throat as post nasal drip (pnd). Sometimes pnd is totally asymptomatic (causes no signs or symptoms),
but more commonly results in frequent clearing of throat or cough. As long as the mucus is moved out of the
sinus continuously (by the cilia - the fine hairs on the surface cells which
move the mucus both from the sinuses and chest) you cannot get a sinus
infection. However, the openings of the
sinuses are very small and the allergic inflammatory swelling of the openings (ostia) can result in narrowing or complete closure of the ostia. When this
occurs, mucus builds up in the sinus cavity.
This often results in a pressure sensation, and if the mucus remains in
the sinus for a prolonged time it becomes purulent (changes color to yellow or
green and smells foul). This purulent colored mucus can ooze out of the
narrowed sinus opening resulting in pnd with bad
breath or colored mucus when the nose is blown.
The retained mucus in the sinus can become infected and this infection
can spread into the sinus lining causing continuous sinus pain usually
localized over the infected sinus, and possible fever (from low grade episodic
to high continuous). A sinus infection
requires antibiotics, and often for a prolonged period time as you must not
only clear the infection from the sinus lining (which has a good blood supply
to deliver antibiotics) but also from the retained mucus (which has no blood
supply and takes much longer to cure).
What has not been appreciated until recently, is that many antibiotics
possess an anti-inflammatory effect and many patients when treated with
antibiotics seem to improve and everyone assumes it was an infection, when
often it is allergic inflammation that is reduced by the anti-inflammatory
effect of the antibiotic. It is very
important not to miss an acute sinus infection as this occasionally can spread
into other tissues with severe consequences. Obviously, promoting good drainage
of mucus from the sinuses is required to clear infection quickly and to prevent
recurrent infections. What is usually
not appreciated is that pure allergic inflammation of the sinus lining can be
interpreted as pain. This pain results
in headaches in the cheeks, between or behind the eyes, in the forehead, and
any headache located in the face in front of the ears must be considered as
being likely sinus in origin.
Individuals with sinus headaches often have totally normal sinus
x-rays. This often leads to this
diagnoses being missed and the headaches attributed to common migraine or
tension. So how can you tell if your
headache is sinus in origin? This often
depends on a group of other findings. If
you have allergies, have had positive skin testing for inhalant allergens,
occasionally have colored sinus discharge or bad breath, have a history of
sinus infection or nasal allergy, etc.-the more of these findings the more
likely your headache is sinus in origin.
Sinus headaches can often cause nausea and vomiting -the old idea that
vomiting always means migraine headache is incorrect. If your facial headache occurs with any other
allergy symptom or if your headache is seasonal - the headache is sinus until
proven otherwise. The other interesting
component of allergic sinus disease is the feeling of extreme unwellness, and many of my patients feel like they have the
"flu ". Ultimately, the proof
is in the pudding, and proper treatment of your allergies and sinuses should
result in a marked improvement in your symptoms. Sometimes it is exceedingly difficult to tell
from the history what is causing a specific facial headache and I will simply
tell the patient - " if you have clear cut positive
skin tests and standard allergy treatment eliminates your headaches, allergy is
the cause ".
Treatment is
quite similar to allergic rhinitis in some aspects. The initial primary treatment is avoidance of
major allergens if at all possible.
Next, it is absolutely essential to use a nasal anti-inflammatory spray
and to use it as per my nasal spray instructions. Several features are critical when using your
nasal spray for allergic sinusitis. The
nasal spray reduces allergic inflammation and swelling in the nose AND sinus
opening (ostia) only if used properly. You cannot sniff too hard or you will pull
the nasal spray into the throat (we are not treating your stomach!!). You should never taste the nasal spray. It should soak into the lining of the side of
the nose. The majority of your sinuses
open into the side of the nose. The
biggest mistake my patients make occurs when putting their head sideways - many
individuals think their head is truly sideways and it is not. If I have any question about the individuals technique, I insist that they put their head
flat on the kitchen table immediately after spraying that same side of the
nose, and they must allow one minute for the spray to adequately soak in. Please read the detailed nasal spray instructions. Often immediately after using the nose spray
you will experience pronounced post nasal drip (pnd),
this is not the nose spray going down your throat (if you followed
instructions), merely represents the nose and sinus lining being stimulated to
produce extra mucus by the act of spraying itself. I developed this nasal spray technique myself
and have used it on hundreds of patients successfully who had previously used
the sprays with little improvement. Details on the safety (they are very safe)
of nasal topical anti-inflammatories are found in the treatment section. Please note that I am not talking about
topical decongestant sprays, as these cannot be used continuously without
causing problems (rebound congestion).
All topical anti-inflammatory nasal sprays are by prescription and
contain corticosteroids. The big difference in treating sinus allergy is the
use of oral decongestants. For allergic
rhinitis antihistamines are often a useful addition. In most adults antihistamines added on top of
your nasal spray do not provide significant additional benefit. (Occasionally, more often in children than
adults, antihistamines are effective in controlling the sinuses. Interestingly, this means that the allergic
process in this individual is primarily of the immediate type, as the mast
cell, the early phase cell, is the cell that releases histamine, which of
course is what antihistamines block.
Another interesting note, is that antihistamines block the histamine receptor,
and are much more effective when taken prior to exposures, prior to the initial
release of histamine from the mast cell, than taken after the initial allergic
reaction when released histamine has already attached itself to the histamine
receptor causing fluid, swelling, itching.)
In most sinus patients oral decongestants are the best additional
medication. Oral decongestants can
decrease the swelling in the sinus lining and ostia
and help decrease mucus secretion. Oral
decongestants can be pure, or can have antihistamines combined with them. I usually recommend a 12 hour oral
decongestant to be taken in the morning, to last the duration of a normal
working-school day. If an individual
gets a sinus headache during the day, I usually recommend adding on top, a
combination of ibuprofen and oral decongestant (30 mg pseudoephedrine) ( i.e. "Advil cold and sinus"). Oral decongestants should not be used in the
evening as they keep most individuals awake or results in extremely light
fitful sleep. Pseudoephedrine has been
shown to rarely increase the blood pressure of individuals who have high blood
pressure-but I always recommend any individual with hypertension (high blood
pressure) should have their blood pressure checked while on pseudoephedrine to
ensure it is OK. Similarly decongestants
can increase the pulse rate, and should be used with caution in individuals
with a history of rapid heart beat (tachycardia) or
palpitations, atrial fibrillation, glaucoma, hyperthyroidism, or urinary
difficulties. Please see the treatment
section for a further discussion of oral decongestants and side effects. Topical nasal decongestants (i.e. DristanTM, OtrivinTM nasal
sprays, etc.) I rarely use except in one
circumstance. If an individual is on
full treatment (avoidance, nasal anti-inflammatory spray, daytime oral
decongestants) and still is having sinus headaches occur in the night, and I am
sure they do not have a sinus infection, I will occasionally recommend the use
of a topical decongestant at bedtime (with the same nasal spray technique as outlined
above) for a short period of time to provide additional decrease in swelling
around the sinus opening. Note, never
should topical decongestants be used twice daily, or rebound congestion rapidly
occurs.
Individuals who
do not respond to standard treatment -avoidance measures and standard
medication -are serious candidates for immunotherapy (allergy shots). This form of treatment is discussed in detail
in the Immunotherapy subsection.
EARS & ALLERGY
Although there
is a fair amount of information on how respiratory allergies can affect the
ears, I am continually amazed at how frequently this information is
overlooked. This is an area seriously
undertreated. The basic anatomy involves
the eustachian tube.
This tube originates at the side and back of the nose. It runs up into the base of the middle
ear. The middle ear is a hollow area
behind the eardrum. When noise hits the
eardrum, it vibrates and this vibration is eventually interpreted as
sound. The function of the eustachian tube is to keep the air pressure in the middle
ear equal to outside air pressure so the eardrum can vibrate normally. Please see the diagram of the eustachian tube and middle ear. The eustachian tube
is an extremely complex structure and the explanation that follows is an
oversimplification, but gets basic information across. If allergic inflammation is causing swelling
in the nose the eustachian tube entrance at the side
of the nose can be involved. The initial
opening of the eustachian tube has the same respiratory
lining. If there is enough swelling of
the eustachian tube entrance, it blocks off. When this occurs a pressure difference occurs
between the middle ear (which is now isolated) and the outside air
pressure. If the blockage is mild little
bits of air can occasionally move through the blocked area when there is
sufficient pressure difference. This
results in the patient experiencing a popping or crackling sensation in their
ear (an attempt is being made to make the air pressure equal between the middle
ear and the outside). This situation
occurs routinely in individuals in airplanes -particularly on ascent or descent
when the change in outside air pressure is rapid. And as many individuals know, this difference
in pressure can cause pain (essentially your eardrum is being pulled inward or
pushed outward and if you stretch the eardrum enough it hurts - a lot!!). In young children the eustachian
tube is much narrower than in adults, and blockage of the tube is much more
common. If a young infant has nasal
allergy the eustachian tube opening is swollen and
narrowed. This sets up the scenario for
recurrent or chronic blockage.
Significant allergic inflammation can by itself cause the eustachian tube entrance to block. This immediately can cause decreased hearing
(the eardrum does not move as well due to the pressure difference) and can
cause pain if the pressure difference is significant. Mucus from the lining of the eustachian tube can build up into the middle ear and the
child now has fluid in the middle ear.
If there is sufficient fluid it will push the eardrum outward, cause a
red inflammed eardrum, and severe pain. Note, this can all be caused by allergy. If the fluid stays the middle ear, over time
the chance that this fluid will get infected increases markedly. If the fluid in the middle ear becomes
infected, this child will instantly have a fever. Now for the most important point, if there is
no fever there is no infection in the fluid in the middle ear. Children who have recurrent " ear infections " with no fever likely have
underlying allergies. What makes matters
worse, is that viral infections add to the swelling in the nose making it more
likely to have eustachian tube blockage, and in many
children "teething" can also have a adverse effect on the eustachian tube (these conditions are additive on top of
the allergic inflammation). Any child
who has three ear infections, constant fluid in the middle ear, or episodes of
ear pain-fluid with no fever, should be assessed for allergies and allergy
tested. The old idea that young children
cannot be allergy tested is wrong, and it is very easy to skin test any infant
over six months of age (provided the parent consents and will hold the child
appropriately during testing). Please
see the section on skin testing for more details.
The treatment
of allergic-eustachian tube dysfunction is similar to
nasal rhinitis. The primary treatment is
avoidance of allergens and irritants. In
infants this particularly applies to dust mites, pets, molds, and the primary
irritant is tobacco smoke. The next step
in treatment is using a nasal anti-inflammatory spray to reduce the swelling in
the side of the nose, to promote opening of the eustachian
tube entrance and drainage of any fluid accumulated. Antihistamines can be useful to decrease
mucus production. Many allergic children
can avoid having multiple courses of antibiotics and a general anesthetic with
placement of tubes in the ears with these measures. Perhaps even more important than this, is
that you have identified the child as being atopic (allergic) and that
institution of proper avoidance measures (i.e. dust free bedroom, smoke free
house, see avoidance section for details) can give this child a significantly
better chance of not developing other allergy related problems (sinuses,
asthma). This represents true
prevention. As these children get older,
the eustachian tube gets larger, and they often
"outgrow" their ear problems by age 3 to 5 years. However, I am seeing more
older children and adults now with this problem, which is in keeping
with the fact that allergies are markedly increasing both in frequency and
severity. Some children have very narrow
eustachian tubes, and despite all measures they fail
to clear the middle ear of fluid (a reasonable time would be within three
months), and these children always require tubes in the eardrum to give them
normal hearing. You cannot allow a young
infant to go many months to years with significant eustachian
tube dysfunction and decreased hearing as this is a critical time for speech
development. I think it's very important
parents understand this concept, that if you apply
proper avoidance measures and medications and the infant still has fluid in the
ear, it must then be dealt with surgically.
However, in my experience most of these children with proper allergy
treatment do not need any further intervention.
Admittedly, I do see a biased population, as parents that bring their
children to me, suspect allergy in the first place (a sibling or the parents
have allergies).
ALLERGIC CONJUNCTIVITIS – THE EYES
In this
section I will discuss the most common problems that allergy causes in the area
of the eyes. I will not discuss rare
allergic conditions that involve the eyes that require treatment and follow-up
by an ophthalmologist.
Allergic
conjunctivitis is the most common allergy eye problem. The conjunctiva is the thin layer of tissue
that covers the inside of the eyelids and then travels over the white area of
the eyeball (the sclera). The conjunctiva does not cover the cornea (the clear
area that you see through). The conjunctiva is part of the eye. When allergy affects the conjunctiva it
virtually always causes significant itching, the conjunctiva usually turns
pink-slightly red (usually the conjunctiva is clear and you see the white of
the sclera), and this can be associated with an increase in clear tear
production. Acute allergic conjunctival
reactions can result in swelling of the conjunctiva which many individuals find
very alarming as it seems as if the eyeball itself is swelling (note: the
cornea is not involved). Classic acute
conjunctival reactions often occur if an individual is allergic to a pet and
the allergy particles that are in the air land directly on the conjunctiva or the
allergy particles often can be on the hand (after touching an animal) and then
brought up to the eye when this individual rubs their eyelids, adjusts their
glasses, etc. Acute conjunctival
reactions often settle within a period of hours. More prolonged conjunctival reactions are
commonly caused by prolonged contact with pollen that is in the air. This produces the typical seasonal symptoms
that can go on for days to weeks during hayfever
seasons. Chronic persistent
conjunctivitis occurs when an individual is exposed to an allergen on a chronic
basis (often persistent daily exposure to pet allergen). Chronic allergic
conjunctivitis often results in more tenacious tear production - the individual
develops clear mucus in the eye which is bothersome and can distort vision
slightly. It is very important to note
that allergic conjunctivitis does not cause purulent colored mucus in the eye
(this is always caused by either a viral or bacterial infections) nor does allergic
conjunctivitis cause pain (pain can be a symptom of much more serious eye
problems). The treatment of allergic
conjunctivitis can be simple avoidance (if touching a cat and then touching
your eye makes your eye itchy you will avoid doing that). If medication is
required oral antihistamines can be effective and topical antihistamine
eyedrops can be rapidly effective for many individuals (read the separate
subsection on how to use Eyedrops).
Antihistamines are always more effective when taken prior to exposure. There are other additional types of eyedrops
that are available for allergic conjunctivitis.
It is also worthwhile noting that the standard corticosteroid nasal
sprays we use for allergic rhinitis can also have a beneficial effect on
allergic conjunctivitis (making sure there is no contraindication such as
glaucoma, viral eye infections, etc.).
If avoidance measures are not practical and medication does not control
your conjunctivitis adequately then allergy shots-immunotherapy is often highly
effective in eliminating these symptoms.
I have
noticed a substantial increase in periorbital
dermatitis over the last few years.
Strictly speaking this problem is not truly an allergy problem of the
eye as the area affected is the skin of the upper and lower eyelids. In this condition the skin of the eyelids
becomes red, itchy, can have a variable degree of swelling, and when the
process is healing can result in the excessive loss of dry scaly skin in the
affected area. There are two common
subtypes and both can severely affect how an individual looks and their self
esteem. The first subtype is a variant
of eczema. This often occurs in
individuals that have patches of eczema elsewhere on their body. Rarely, this can be the only area where the
eczema is active. Allergy can directly
drive this process where direct contact with pollen, pet allergen, wood dust,
etc. can affect the skin around the eyes.
However, as with eczema in general, other factors than allergy can also
drive this process. Please read the
subsection on eczema for a more detailed discussion. Treatment for this subtype is exactly the
same as for eczema elsewhere on the body.
The second subtype is allergic contact dermatitis. This form of allergy is usually not IgE
mediated and is often a form of delayed cellular immune response (similar
cellular immune responses can be seen in individuals who are allergic to metals
contacting the skin (nickel and chromium being the most common allergens) and
in poison ivy). It is important to diagnose this kind of allergic reaction as the
typical delayed cellular immune response often takes weeks to complete
(classically starts with a red itchy skin, the skin of the eyelids can then
swell up, possibly develop blisters, then the skin gradually heals (swelling
and redness disappear) while there is a significant loss of dry skin scales in
the healing area. Common causes of this
type of allergic reaction are many forms of eye makeup, facial makeup, acrylics
(particularly acrylics used in nail polish), components of eyeglasses, and any
other allergenic compound that could be touching the eyelid area. Identifying the causative allergen is
critical as this will reaction will continue until the offending allergen has
been avoided for several weeks. If the
specific cause of the reaction cannot be found by history, I usually initially
eliminate all makeup for a period of one month.
If the eyelid dermatitis disappears, then each specific eye/facial
cosmetic is added back in one at a time to determine the offending agent. Individuals who become allergic to specific
facial cosmetics should use as little makeup as possible and always use the
same brand of makeup that does not bother them (although manufacturers can
change composition). Hair dyes can cause
periorbital dermatitis but usually the scalp is
involved in the reaction and the diagnosis is usually easily made (the reaction
starts immediately after dye application).
Delayed cellular immune reactions can be proven by patch testing with
the suspect allergen on the forearm for a period of 1-3 days.
A discussion
of allergy problems in the eye area would not be complete without talking about
allergic shiners (also discussed in the allergic rhinitis section). Allergic shiners involve only the lower
eyelid and typically involve this area becoming dark and swollen (puffy). This can occur seasonally in people with hayfever, episodically in individuals whose allergies wax
and wane, and chronically in individuals with persistent allergic
rhinitis. The blood supply of the lower
eyelid drains partially through the nose - when the nose is affected by allergy
the lining of the nose swells up and becomes inflamed (allergic rhinitis) and
this swelling impedes the flow of blood away from the lower eyelids causing
these areas to become dark and swollen.
Identifying allergic shiners gives you a good way to follow nasal
allergy (parents can identify how their child's nasal allergy is doing simply
by looking for allergic shiners). Many
individuals erroneously attribute allergic shiners to not getting enough sleep/fatigue,
but this cause never results in swelling of the lower eyelid (in fact the area
often looks sunken) and only occurs with significant sleep deprivation,
malnutrition, etc. If a person has
allergic shiners and also a stuffy nose it's a pretty safe bet you're dealing
with allergy.
ALLERGIC LARYNGITIS & TRACHEITIS
I will spend
little time on these two entities. I do
think it is important that you are aware of these. Both should be suspected if you develop these
symptoms seasonally. In allergic
laryngitis, the individual breathes in particles they are allergic to and when
the particles land on the vocal cords (larynx) they develop allergic
inflammation and a subsequent change in voice/pitch or loss of voice. Be particularly suspicious of allergy if
there is no overuse of the voice (yelling, singing, etc.) or evidence of viral
infection. Many of my allergy patients
get mild allergic laryngitis very rapidly on exposures to certain allergens
(often mold spores) or some irritants (tobacco smoke, etc.). Unfortunately, we do not have any specific
topical therapy for this area. The best
treatment is avoidance of allergens and irritants that trigger the laryngitis,
and resting the voice if it develops.
Occasionally, antihistamines can be useful in high dosage, particularly
if taken prior to exposure to prevent allergic laryngitis. I should also mention that using inhaled
anti-inflammatory corticosteroids for asthma can cause a hoarse voice if a
spacer is not used properly with puffers and/or proper gargle and rinse procedures are not
done after inhaler use. Allergic tracheitis presents as a dry cough only, often seasonal in
nature, lasting several weeks with no evidence of infection. The cough is often made worse with exposure
to cold air or irritants but never causes true shortness of breath. It's not unusual to have mild central chest
discomfort with this entity and you have to be careful in older individuals to
rule out heart disease. However,
allergic tracheitis does occur, and in many individuals
I have followed for years, eventually true asthma has developed (the allergic
inflammation has moved down further into the smaller tubes in the lungs). The treatment of allergic tracheitis
is identical to asthma, as anti-inflammatory inhalers do a good job, and often
treatment is only required seasonally.
Individuals with allergic tracheitis have
consistently normal lung function, with or without symptoms.
ASTHMA
There are huge
resources available regarding asthma.
For a detailed discussion of asthma, GINA (the Global Initiative for
Asthma) is excellent and any of the national asthma programs (
Although the
vast majority of asthma is initiated by the allergic inflammatory process, and
many individuals continue to have their asthma driven by allergy, there are
small sub groups that do not fall into this category. As we have already discussed, asthma is a
chronic inflammatory process that occurs in the medium and smaller tubes of the
lung. This inflammatory process results
in the tubes becoming overly sensitive to a variety of allergic, irritant, and
physical stimuli. When these tubes are
exposed to one or more of these stimuli they narrow down. This narrowing of the tubes results in
difficulty breathing, shortness of breath, or wheezing. One of the characteristics of asthma is that
this narrowing (bronchocostriction) is reversible
either spontaneously or with medication.
For many years the diagnosis and treatment of asthma concentrated on the
bronchocostriction aspect of asthma. We now realize that the basic underlying
process is inflammation within the tubes in the lung and the current treatment
of asthma focuses on reducing and controlling this inflammatory process. If the inflammation in the tubes is well
controlled the asthmatic will have minimal to no symptoms. We also know that this inflammatory process
is not benign for some asthmatics can result in permanent damage to these tubes
(i.e. scarring in the tubes and permanent changes such as an increase in muscle
tissue in these tubes, which is called remodelling,
which results in a permanent loss of lung function). Some individuals with asthma lose lung
function faster than normal individuals/many asthmatics and this lost lung
function is not retrievable. This is why
it is so important to begin the treatment of asthma with anti-inflammatories
early in the process to not only reduce or eliminate symptoms but to attempt to
reduce loss of lung function through a comprehensive approach by treating
asthma, treating other concomitant allergy problems (nose, sinus, skin),
appropriate allergen avoidance measures, immunotherapy (allergy shots), etc. A concept I want you to retain regarding
asthma treatment is that eliminating the bronchocostriction
results in improved airflow through the tubes and an improvement in lung
function, but if we reduce the inflammatory swelling in the tubes, this results
in a further improvement in lung capacity and function and decreases the
frequency and severity of episodes of bronchoconstriction. Another concept I want you to have is how
chronic asthma is; even if there are no symptoms, this inflammatory process
usually continues. I like to compare
asthma to an engine with an unlimited fuel supply. Allergy is the process that turns the engine
on in children and most adults (occasionally in adults major chemical exposures
can do this, and occasionally viral infections likely can do this also). Once the engine has been turned on it
continues to run on its own. We do not
have the key to turn the engine off. If
the engine is idling the individual has few symptoms. Subsequent exposures to allergens (things the
asthmatic is allergic to-particularly airborne allergens) or viral infections
step on the accelerator, speed the engine up, and create more symptoms. With proper allergy avoidance measures and
appropriate anti-inflammatory treatment, the engine will tend to always idle.
So why has it
proved to be so difficult to treat asthma?
There are numerous studies that show asthma is consistently under
diagnosed and under treated. We also
know there has been a huge increase in the incidence of asthma and the severity
of asthma throughout all age groups.
This has huge implications for the future. There is a significant hereditary aspect to
asthma. If one or both parents have
asthma, the risk of asthma is significantly higher in the child with mom
tending to pass down a higher risk to each of her children. Asthma is a highly variable disease. It can start in very early infancy with
obvious episodes of wheezing. Often this
is seen with viral infections and children with asthma often tend to have
prolonged symptoms (wheezing, coughing, difficulty breathing) after a
cold. Many young children who were
diagnosed as asthmatic, will "outgrow" their asthma in later
childhood and continue into early adulthood with no symptoms. However, these individuals usually have
abnormal pulmonary function testing (PFT) and often develop asthmatic symptoms
in later adulthood again. Many young
infants wheeze with viral infection simply because the infection itself causes
inflammation and swelling in the tubes which results in wheezing. Remember, wheezing is a high pitched
whistling sound that comes from the chest and is caused by the small and medium
sized airways being narrowed by any cause.
Although, wheezing has other causes, it still remains the single
symptom, that when present over time is clearly associated with the correct
diagnosis of asthma. The initial
symptoms of asthma are highly variable.
Sometimes the only evidence of asthma is coughing. The cough often occurs at night with the
child clearly having no viral infection or on exposure to cold air, exercise,
or emotional extremes (i.e., laughing, crying, anger, etc.). In young children we cannot do any formal
testing to prove asthma exists. The
diagnoses in young children rests on symptoms, having a high suspicion (i.e.
parents who have asthma, family history of allergy), having clear cut
significant positive skin tests (children and most adults with asthma have very
significant positive skin tests), and a clear cut response to wheezing with
treatment (using openers to reverse bronchoconstriction) or a response to all
symptoms with anti-inflammatory medication (inhaled steroids). In older children (5 to 6 years old) and
adults it is somewhat easier to make the diagnosis. Everything mentioned already applies, but now
you can do lung function testing (PFT-pulmonary function testing,
spirometry). In undertreated or
untreated asthma you can often see evidence of asthma on an initial PFT (the
FEV1 (ability to move air out of the chest in one second) is often reduced well
below expected value for that individual, particularly in relation to total
lung capacity (FVC)). A standard
definition of asthma for many, is that the FEV1 must improve by 15 to 20% after
using a bronchodilator medication (opener, beta agonists). However, this creates a real problem. What do you call the individuals who only
improve 12% or 9% (you get the picture).
They still have inflammation in their tubes. This definition of asthma is convenient for
asthma studies, but does not include many individuals who require treatment
(especially milder asthmatics). Another
way to diagnose asthma is to measure lung function (do a PFT) then deliberately
irritate the tubes by breathing in a substance that usually irritates the tubes
of asthmatics (a methacholine or histamine challenge) and demonstrating
narrowing of the tubes (a decrease in FEV1 of 15 to 20%). While this is usually positive in asthmatics,
it still likely misses some individuals with mild inflammation and can be
positive in individuals who do not have asthma.
Many asthma experts require a positive methacholine challenge to call
the disease process asthma. However, I
feel the best way to diagnose asthma in individuals who are suspect, is to
document an improvement in PFT and symptoms over time by instituting proper
avoidance measures and treating the individual with anti-inflammatory
medication. This concept is critical;
that repeat PFTs over time will show an improvement. It's important for any asthmatic to
understand, that a PFT done at any given moment, only reflects the inflammation
in their lungs at that specific moment, and that their PFT varies over time
just as the amount of inflammation varies over time. Another less accurate way of assessing lung
function is the peak flow meter. This
instrument is inexpensive, portable, and can be used by the asthmatic at home,
and measures the peak expiratory flow rate (PEF). While this is useful for some asthmatics
(particularly asthmatics who do not perceive changes in their lungs or parents
of younger children who cannot tell their parents how their chest is) it has
certain major drawbacks. The readings
are highly dependent on consistent technique (a major problem with some
children) and effort and the PEF measures the airflow through the larger
tubes. A peak flow meter is a useful
instrument for any asthmatic or parent provided they wish to use it. However, compliance in taking medication
regularly is a huge problem and using a peak flow meter represents another
activity the asthmatic has to do, and for a large group of asthmatics is not
absolutely essential as long as the asthmatic can maintain good control of
their asthma continuously.
Making matters
even more difficult, is that asthma likely represents a group of inflammatory
disorders. By this I mean that it is
likely that there are basic differences in the inflammatory process in certain
groups of asthmatics. All asthmatics
have chronic inflammation, but there is mounting evidence that certain
asthmatics differ from others in the type or relative amounts of certain
inflammatory cells (and the chemicals they release) and this is why some
asthmatics will respond better than others to a specific medication. Taking all this into consideration, the fact
remains that many asthmatics remain undiagnosed or undertreated.
Once asthma has
been diagnosed, the treatment should be straightforward. Once again the primary treatment is avoidance
of allergens and irritants that drive the inflammatory process in the
tubes. A special mention should be made
about specific entities. In the large
majority of children with asthma, dust mite allergy drives the allergic process
and the child's asthma. In individuals
who are allergic to dust mites (proven by skin testing), eliminating exposure
to dust mite allergen in the bedroom particularly (the dust free bedroom, see
this in the avoidance section) reduces the asthmatics symptoms and medication
use in the long term. Dust mite allergy
is a chronic driving force behind allergic inflammation. Particularly, there is evidence that strict
avoidance of dust mite allergen in young infants and children can reduce the
development of respiratory allergic disease (asthma, rhinitis, sinusitis). This is
very important, as we can prevent the development of asthma in some children
(and likely reduce the severity in the rest) with simple avoidance
measures. We know that exposure to
tobacco smoke (primarily an irritant, with over 4000 separate chemical components)
increases the risk and severity of asthma.
No child should be exposed to second hand tobacco smoke, and
particularly no child with a family history of allergies or asthma should ever
be exposed to second hand tobacco smoke as we know this irritant causes more
severe symptoms in allergic individuals.
Exposure to environmental tobacco smoke (ETS) can double a child's risk
of asthma. All smoking parents (and
relatives, friends) must always smoke outside the house and never in enclosed
spaces (like the family car). A special
mention should be made about molds. For
a detailed discussion on mold spores, see the section on Allergens &
Irritants. We know that young children
who are allergic to mold spores diagnosed by skin testing) tend to have more
persistent and severe asthma. Reduction
of mold spores and dust mite and pet allergen requires removal of carpeting, as
carpets represent a major reservoir for these allergens. Cleaning any areas that are obviously moldy
and keeping the house dry are also essential.
Significant mold contamination requires removal of all affected housing
material using appropriate protection precautions. In children who are allergic
to cats or dogs (or other pets, again diagnosed by a clear exposure history and
skin testing) exposure to this allergen also drives the allergic inflammatory
process, increasing the risk of developing and the severity of asthma. Removal of the pet is clearly the best
solution as it takes many months even after pet & carpet removal and appropriate
washing to eliminate allergens from the house.
Details can be found in the Avoidance subsection. If the pet cannot be removed extensive pet
control measures will be required for pet allergic individuals (see the Pet
Control Measures subsection).
Next, we want
to use anti-inflammatory medication to get the inflammatory process under
control and then control the chronic inflammation well to prevent symptoms from
appearing. The fast acting openers (beta
agonists) should be used whenever an asthmatic feels there chest is tight, is
short of breath, or wheezing. The use of
your opener is a good measure of asthma control. When you have a viral infection many
asthmatics will require their opener frequently (perhaps every 4 hours) and if
you need it, you use it. For specific
details on all these medications see the Medication section. However, good asthma control is attained (in
other words you are controlling the inflammatory process well) if you use your
opener once a week or less and in the majority of asthmatics this is attainable
with a combination of proper avoidance measures and appropriate
medication. Initially you use high
dosage anti-inflammatories to get the inflammation under control. This means you use oral prednisone or high
dosage inhaled corticosteroids. The
mistake often made is that as soon as symptoms (wheeze, cough, etc.) have
disappeared the anti-inflammatory medication is reduced too early. Prednisone is only used for the acute flare,
usually 7 to 14 days worth (except in a few of the most severe asthmatics who
may require regular prednisone for adequate control). However, high dose inhaled corticosteroids
(which are safer), should be continued for a period weeks-months to get the
process under good control, prior to reducing the inhaled steroid dose. We know that when symptoms disappear, the
inflammatory process lags at least six to eight weeks behind before settling
back to well controlled minimal inflammation. In many asthmatics who are undertaking
avoidance measures for the first time or have significant seasonal or
occupational exposure it takes many months to get the inflammatory process
under control (it's not unusual for this to take six months to two years) and
only when the inflammatory process is under good control should you decrease
your inhaled steroids to low dose. We
determine good control by a lack of symptoms and an improved and stable
PFT. In the long run, we want the
individual to be on low dose inhaled corticosteroids, as we know this is
safe. Even low dose inhaled steroids can
prevent scarring (loss of lung function) in most asthmatics. We want to avoid the long term side effects
of high dose inhaled steroids (small but increased risk of osteoporosis, thin
bruising skin, glaucoma, cataracts).
Another way of looking at long-term steroid use, is that the majority of
the beneficial effect of inhaled steroids (reducing frequency of flares
&hospitalization, improving lung function, improving quality of life, etc.)
is attained at low doses and increasing the long term dose of inhaled steroids
above low doses increases the side effects of the steroids without providing
significant further improvement in asthma control. Remember, we are controlling an inflammatory
process that if not controlled can permanently damage the lungs resulting in
loss of lung function. There is a group
of very severe asthmatics that appear to continue to lose lung function despite
using all available medications (including steroids). Should asthma symptoms not come under rapid
control with the above measures, the next step is to add in an additional
anti-inflammatory. We now have available
the leukotriene receptor blockers (Accolate, Singulair) that have
anti-inflammatory and opener (bronchodilating)
properties. One of these medications
should be tried in addition to continuing inhaled steroids. These medications work very quickly, usually
effect is seen within two days, and if effective can allow a more rapid
reduction in inhaled steroids.
Unfortunately, these leukotriene receptor blockers only work in
approximately half of the asthmatic population (it is genetically determined -
you either do or do not respond). When
they do work, they allow a significant reduction in long term inhaled steroid use
and also have beneficial effects on the upper airways (nose,sinuses). The
improvement in asthma with leukotriene receptor blockers should result in a
significant reduction in symptoms and proven by an improvement in lung function
(PFT). These new medications are
expensive, have a good safety profile, and if one leukotriene receptor blocker
does not work, it is very likely the other will not work also. If there is no response to the leukotriene
receptor blockers the next step is usually to add in a long acting opener which
can improve asthma control (long acting beta agonists - LABAs: OxeseTM, SereventTM (or their
respective steroid combinations SymbicortTM, AdvairTM, ZenhaleTM). These long acting openers are taken every 12
hours and have been shown to reduce asthma symptoms while improving lung function
and quality of life. LABAs when used
regularly must always be taken with an inhaled steroid (used alone regularly
they can increase the risk of severe/fatal asthma attacks). So far these long acting openers have also
been shown to be safe, with minimal side effects (tremor, increased pulse,
headache being the commonest). Long
acting openers -LABAs do not possess any anti-inflammatory properties, do not
improve upper airway symptoms, but do work for all asthmatics. I feel it makes imminent sense to treat the
basic inflammatory process maximally (with proper avoidance and
anti-inflammatories), before using other medications. At this point, most asthmatics (well over
90%) should be under good control and using their as necessary short acting
beta agonist (opener) less than once per week, exercising normally, and having
no asthma symptoms that interfere with work, pleasure, or sleep. Excellent control is achieved when an opener
use is less than once per month.
In asthmatics
still not under good control, there are other medications that can be tried
(i.e. theophylline). A new monoclonal
antibody to IgE has become available (omalizumab-“Xolair”TM), but is very expensive and only applicable for a
small minority of severe allergic asthmatics.
Also, consideration can be given, in asthmatics who have clear cut
unavoidable allergy driving their asthma, to immunotherapy (allergy shots).
However, and this is a huge however, asthmatics who have not come under control
with the above measures usually are not following their treatment plan. Many asthmatics do not comply with proper
avoidance measures. I strongly feel
every asthmatic should be allergy tested to identify the specific allergens
they have to avoid and to be properly educated in proper avoidance measures and
equipment. It is not appropriate to tell
an asthmatic to get rid of pets, carpets, etc. without the objective proof of
specific allergy determined history and appropriate skin testing. I would encourage you to read the section on
allergy skin testing as this must be done properly and if done incorrectly can
cause significant long term problems (particularly if the patient is told they
have no allergies). This being said,
many asthmatics do not practice proper avoidance measures. The bedroom remains a source of dust
mite-mold-animal allergen, the pet they are allergic to remains in the house,
and so on. You cannot expect good asthma
control with continuing exposures to major allergens. Compliance with medication use is also a huge
problem both from the physician and patient point of view. There still are physicians who are hesitant
to prescribe inhaled steroids and particularly a large number who use steroids
intermittently. The intermittent use of
steroids is unacceptable for most persistent asthmatics. The exception to this will be discussed
below. Many patients fear the word
steroid and corticosteroids are anti-inflammatories and are not to be confused
with anabolic steroids. While long-term
prednisone use and high dose inhaled use clearly have detrimental long-term
effects (prednisone far more so than inhaled) the short term use of these
steroids (prednisone for two weeks or high dose inhaled steroids for several
months) is quite safe. Low dose maintenance
inhaled steroids are exceedingly safe.
Nonetheless, many patients do not take these medications regularly (some
never take them) and the inflammatory process is never adequately controlled. Many studies have shown patients routinely do
not admit to physicians that they are not taking their medication
properly. Another sadly overlooked area
is that of inhaler technique. Many
studies have shown that the majority of patients, physicians, and pharmacists
do not have or remember correct inhaler technique. You cannot expect the asthmatic to use their
inhalers properly if they have never been shown how to do it correctly. Moreover, many studies have shown that even
with correct initial technique, many patients subsequently fall into incorrect
technique over time. The most difficult
asthmatic patients are individuals who have had asthma for years and know how
to do everything correctly. They don't
realize that the treatment of asthma, including inhalers, technique, and
medication continually is evolving with new understanding and better
equipment. This is where patient and
physician education is critical, for only if you realize this field is
constantly progressing and improving with time, and only if this translates
into increased knowledge will you get optimal treatment and then get optimal
results. When all this has been taken
into account there remains several specific things that can continue to drive
asthma and cause poor control. Ongoing
allergic inflammation in the nose makes asthma worse (primarily through a nerve
reflex, making the nerves that supply the lungs overactive, and contributing to
narrowing (these are the same nerves that cause an asthma attack when you
laugh, cry, etc.)). Allergic sinusitis
(with or without infective sinusitis) always drives asthma and must be
treated. Pnd
(post nasal drip) may worsen some asthmatics but more commonly causes
cough. A badly overlooked area is acid
reflux. This term reflux refers to acid
from the stomach moving back up the esophagus (the tube you swallow food
down). There is an exceptionally high
amount of reflux in asthmatics. What is
interesting is that over 30% of patients with significant reflux have no
-that's zero -symptoms of heartburn.
Although, the occasional patient with reflux is so severe that the acid
travels all the way up the esophagus into the back of the throat (directly
irritating the airway), in the vast majority of people with reflux the acid
irritates the nerves of the lower esophagus (remember no symptoms necessary)
which causes an increase in the nerve input to the lungs and consequent
increase in irritability of the tubes of the lungs. If reflux is suspected as a contributing
factor in difficult to control asthma a trial of medication to reduce acid
production in the stomach is warranted.
A positive trial for reflux would improve asthma symptoms and improve
the PFT (while holding all other variables constant). In this context, only our most powerful acid
reducing agents in maximum dose should be used for this trial, intermediate
acid reduction agents are not appropriate.
Some brief
comments on inhalers are appropriate.
The most common inhalers are the MDIs (metered dose inhalers) or the
"puffer ". Most inhaled
steroid puffers must be used with a spacer device (AerochamberTM,
etc.). These spacer devices reduce the
amount of residual steroid in the mouth and allow for improved deposition in
the tubes of the lung. Using a puffer
alone you get approximately 6% of the total dose in your lungs, while using a
spacer and puffer you get approximately 15% in your lungs (although this varies
between spacers). These numbers changed
with the elimination of
CFC propellant in MDIs (which now use HFA as a propellant). Most require that you shake your puffer
vigorously before each puff to get an adequate dose, and if you have not used
your puffer in two days you will not get full dose on the first puff. Once your inhaler is adequately shaken and in
the spacer you breathe out, put your lips over the spacer mouthpiece, and press
down firmly on your puffer and start breathing in at the same time. Note: you must breathe in slowly and steadily
(over approximately 2 to 3 seconds) and fully to get optimal deposition (and be
standing to take a full breath in). You
must hold the puff in your chest for a minimum of 6 seconds – I prefer 10
seconds or as long as you can. Holding
less than 10 seconds results in medication being lost as you breathe back out
(exhale). Everyone, particularly adults,
should check their hold time with a watch to ensure you are continuing to hold
for 10 seconds. Young children are very
good once they know how to count 10 seconds on the clock. Adults and teens are always in a hurry. You repeat this technique for every single
puff. After inhaling steroids, you must
take a good mouthful of water, gargle deeply, rinse the mouth, then spit out. The
inhaled steroid should only be deposited in your lungs. Using an opener puffer alone, which is what
everyone does away from home as they don't want to take their spacer with them,
is not a major problem, as less than optimal inhaler technique can be
compensated for by taking an extra puff.
All I will say about this technique, is that you should use your mouth
as the "spacer" and you must inhale faster (approximately 1 second)
to capture the opener medication. Timing
is critical as you should press on the puffer just as you start your breath in.
We now have available multiple dry powder inhalers. All these dry powder inhalers require the
individual to pull the powdered medication into their lungs. Many of these inhalers are more efficient
(for example, the TurbuhalerTM (Symbicort,Pulmicort, Bricanyl, OxeseTM) can deposit 30% of the inhaled medication in the
lungs with proper technique). These
medications contain no CFCs so are environmentally friendly also. All these dry powder inhalers (TurbuhalerTM, DiskusTM, AsmanexTM, etc.) require the patient to breathe out as far
as possible (exhale completely), get a very tight seal over the mouthpiece with
their lips, then inspire (breathe in) as hard and long as possible (you want to
generate as high an airflow rate through the device as you can and continue to
inhale through the device until your lungs are completely full of air & you must be standing to generate a full
breath in), and you once again hold the
medication in your lungs for 10 seconds before exhaling. Similarly, all inhaled steroids require a
good gargle-rinse afterwards. You must
be very careful not to breathe into (exhale into) these devices just as you are
getting ready or you will blow the powder away.
Further comments on specific inhalers are in the medication
section. Probably, the most important
thing to remember regarding inhalers, is that each specific inhaler device,
spacer, etc. has its own unique properties and most require a specific unique
technique to use optimally.
Reprinted
with permission,Dr. Bruce
Sweet, 2014