Wednesday, 3 September 2008



Asthma is an extremely important disease to learn about for several reasons. It is common, affecting young and old. Its prevalence is increasing too. It can lead to a terrible quality of life, and can kill. In addition, it has an extremely interesting pathophysiology that highlights an incredible degree of interplay of many different factors, and a great deal of what a theist like myself would regard as incredible intelligent design. All of these make it one of the most interesting diseases to discuss; it is a great cause of reflection.


Asthma is common enough as it is, affecting an estimated 4 to 7% of people worldwide.. It is believed that, “300 million people world-wide suffer from asthma and an additional 100 million may be diagnosed with asthma by 2025”.

Thus, its prevalence is increasing, as the following diagram shows. According to the World Health Organization (WHO), “8% of the Swiss population suffers from asthma today, compared with just 2% some 25–30 years ago”. In the USA, as the most recent edition of the ‘Merck Manual’ describes:

“More than 20 million people in the US are affected. Asthma is one of the most common chronic diseases of childhood, affecting more than 6 million children; it occurs more frequently in boys before puberty and in girls after puberty. It also occurs more frequently in blacks and Puerto Ricans. Similar estimates are given for other Western nations”.

The reason for this is unclear. Indeed, some authors debate “whether this is due to an actual increase in incidence or merely to the fact that the size of the overall population is growing”. But assuming that it is a true increase, as most commentators believe it is, we must try to find out the reasons for this increase.

Since the aetiology of asthma is as yet poorly understood, it is epidemiological studies that will shed the most light on this. We need to find out what things have increased in the past 30 years or so, that could possibly be related to this increase.

According to several well established studies based on these premises, the increased prevalence of asthma could be related mainly to two things – increasing urbanisation, and the increased prevalence of Westernisation.

I actually mentioned the concept of urbanisation, and its impact on asthma in a previous essay (‘On the Problem of Evil in Medicine’). I quoted a publication in the Lancet, which said:

“Fossil fuel combustion is partly to blame for increased childhood asthma, according to a report published by Harvard Medical School's Center for Health and the Global Environment. But the resulting air pollution is just part of the problem. Increasing temperatures encourage growth of moulds and fungi, and higher carbon dioxide levels stimulate plants to produce more pollen earlier in the year.

Childhood asthma in the United States rose by 160 per cent between 1980 and 1994. Inner city children are at special risk as diesel particles are particularly effective at delivering pollen to immune cells in the lungs, according to the report, called Inside the Greenhouse.

The report advocates local initiatives, such as tree-planting and improved public transport, to reduce greenhouse gases.”

Urbanisation means a lack of, or even loss of contact of man with nature, as well as contamination of the environment with pollution and toxins that lead to the greenhouse effect. As John Rees explained in a BMJ article on the ‘Prevalence of Asthma’:

“The movement of racial groups with a low prevalence of asthma from an isolated rural environment to an urban area increases the prevalence in that group, possibly because of their increased exposure to allergens such as house dust mites and fungal spores or to infectious agents, pollution, and dietary changes…. Symptoms of asthma are made worse by atmospheric pollution such as nitrogen oxides, sulphur dioxide, and small particulate matter. However, outdoor environmental pollution levels do not correlate with changes in prevalence. Indoor pollution from nitrogen oxides, organic compounds, and fungal spores may be more important.”

In addition, it is widely believed, as stated in one of the best selling medical textbooks of our time, ‘Davidson’s Principles and Practice of Medicine’, “The prevalence of asthma increased steadily over the latter part of the last century in countries with a Western lifestyle”. In particular, the increase has been linked to “the rise of obesity in Western society through mechanical mechanisms such as gastro-oesophageal reflux”. Professor Neville Woolf put it brilliantly in his best selling pathology textbook, ‘Pathology : Basic and Systemic’:

“What is of interest is the fact that certain communities (e.g. in Papua New Guinea) previously had a very low prevalence of asthma which, with the advent of the somewhat mixed blessings of Western ‘civilisation’, has increased sharply”.

Other factors believed to be associated are maternal smoking in pregnancy and during the first few years of life, and reduced incidence of breast feeding.

Thus, based on all of the above, we can reiterate the truth of God’s statement:

“Corruption doth appear on land and sea because of (the evil) which men's hands have done, that He may make them taste a part of that which they have done, in order that they may return” (30:41).

I cannot help but requote Muhammad Asad’s very insightful commentary on the above verse:

“Thus, the growing corruption and destruction of our natural environment, so awesomely - if as yet only partially - demonstrated in our time, is here predicted as “an outcome of what men’s hands have wrought”, i.e., of that self-destructive - because utterly materialistic - inventiveness and frenzied activity which now threatens mankind with previously unimaginable ecological disasters: an unbridled pollution of land, air and water through industrial and urban waste, a progressive poisoning of plant and marine life, all manner of genetic malformations in men’s own bodies through an ever widening use of drugs and seemingly “beneficial” chemicals, and the gradual extinction of many animal species essential to human well-being. To all this may be added the rapid deterioration and decomposition of man’s social life, the all-round increase in sexual perversion, crime and violence, with, perhaps, nuclear annihilation as the ultimate stage: all of which is, in the last resort, an outcome of man’s oblivion of God and, hence, of all absolute moral values, and their supersession by the belief that material “progress” is the only thing that matters”


And with this increasing ‘corruption’ so to speak, the consequences are endless. The one thing that sticks to people’s minds the most about a disease is its impact on the economy, and people’s lives.

Perhaps it suffices here to say that one of the most important medical textbooks of our time introduces its discussion on asthma quite simply with the words, “Asthma is a very common disease with immense social impact”.

The most important aspect to know about asthma is that it kills. This was something well known to our elders. For instance, in 1674, Thomas Willis (of ‘circle of Willis’ fame) remarked that:

"Among the Diseases whereby the Region of the breath is wont to be infested, if you regard their tyranny and cruelty, an Asthma (which is sometimes by reason of a peculiar symptom denominated likewise an Orthopnoea) doth not deserve the last place; for there is scarce any thing more sharp and terrible than the fits there of Breathing, whereby we chiefly live, is very much hindered by the assault of this disease, and is in danger, or runs the risk of being quite taken away."

And the fact that it can kill anyone, of any age was equally well known to William Heberden, who remarked that:

“The first fit of the asthma has been experienced at all times, from the earliest infancy to extreme old age, and in every intermediate stage of life”.

To this day, asthma kills over 1400 people in the United Kingdom, and 4000 deaths in the USA, with the death rate being “5 times higher for blacks than for whites”.

Furthermore, it is the leading cause of hospitalisation for children in the Western world, and a leading cause of hospital admission for adults too. Asthma UK, a society concerned with asthma care in the UK, estimates that there are “over 69,000 hospital admissions for asthma each year - 40,000 adults and 29,000 children. This equates, on average, to one hospital admission for asthma every 7.5 minutes”.

This is not to speak of its socioeconomic impact, because of its being “the number one chronic condition causing school absenteeism” and leading to at least 13 million work days lost each year in the UK. In the USA, it is estimated that, “in 2002, the total cost of asthma care was $14 billion,” and in the UK, the cost of asthma to the NHS was over £889 million. The total cost of asthma to the UK economy exceeds £2.3 billion a year (Asthma UK).

All those figures are bound to, or at least should raise a few eyebrows. They should stimulate health care professionals to give preventative advice, and all people to care a little more about the environment. Is it fair that we should destroy the world, and the health of future generations because of our desires (e.g. to smoke (and in the case of many women, smoke particularly during pregnancy), burn away rainforests, the lungs of the earth and adopt the worst eating habits).


The pathophysiology is asthma is quite incredible. Contrary to common conception, it is not simply a disease of ‘reversible bronchospasm’. It is much more than that[1], and highlights an incredible degree of irreversible complexity within the lungs, and a high degree of intelligent design.

The above diagram, from ‘Davidson’s Principles and Practice of Medicine’, illustrates a very important point – that the integrity of all the above structures is important for the stability of the lungs. Someone once described asthma in the ‘Journal of the American Medical Association’ as “a disease that has practically the same symptoms as passion except that with asthma it lasts longer”. This fiery passion is only set alight when the above is disturbed, beginning with the two key cells in the pathophysiology of asthma – the mast cell (a basophil resident in airways and other tissues) which is responsible for the immediate reaction is asthmatics, and the eosinophil, which is responsible for the delayed reaction in asthmatics.

Before we delve into the pathophysiology of asthma, it is important to know that there are two main types – an intrinsic and an extrinsic variant. The intrinsic variety is associated with what is known as atopy – the tendency to produce excessive amounts of the antibody IgE in response to common environmental proteins (such as house dustmite, grass pollen, and food allergens), which are harmless to non-atopic individuals; the reaction is ‘atopic’, from the Greek ‘atopos’, meaning out of place. The extrinsic variant occurs in non-atopics and mast cell activation is provoked by a number of different things, such as drugs, emotion, cold air, exercise and other irritants. The following diagram summarises the differences between the two:

What this knowledge should spring is a great appreciation of the normal self. The asthmatic is the exception, not the rule. The majority of us have normal airways, normal amounts of eosinophils and basophils (mast cells), and IgE (which although still not fully understood, is believed to be involved in the immunity against parasites[2] and possibly cancers), and do not suddenly become asphyxiated by a jog, a stressful situation, or a cold breeze. Let that be at the forefront of your mind should you go out for a jog on a cool summer morning, and be thankful to your Lord for the fact that you are not asthmatic.

The antigen, whatever it may be, is perceived as a dangerous foreign body. The immune system of asthmatics is hypersensitive; it is passionate, moving at the slightest stimulus, even cold air. It is this reaction that led psychologists in the past (mistakenly of course)to regard asthma as a ‘psychosomatic illness’. As Melissa Opolski and Ian Wilson explain in an article published in the ‘Journal of Clinical Practice and Epidemiology of Mental Health’ (2005; 1: 18), ‘Asthma and depression: a pragmatic review of the literature and recommendations for future research’:

“The association between asthma and psychological factors has been recognised for centuries. Asthma has long been considered a psychosomatic disease, and during the 1930s–50s, was even known as one of the 'holy seven' psychosomatic illnesses. At that time, psychoanalytic theories described the aetiology of asthma as psychological, with treatment often primarily involving psychoanalysis and other 'talking cures'. As the asthmatic wheeze was interpreted as the child's suppressed cry for his or her mother, psychoanalysts viewed the treatment of depression as especially important for individuals with asthma”

I reemphasise the point that we ought to be grateful, day in and day out, for the control of our immune systems, the fact that it is so well regulated in the majority of us who do not suffer from autoimmune or allergic disease – two instances of hypersensitivity.

Once the foreign body first enters the system, plasma cells perceive it and produce large amounts of IgE antibody against it. These antibodies attach to mast cells in body tissues and to circulating basophils (via their Fc portion). This situation is stable, until a subsequent exposure to the same allergen. This then combines with the IgE attached on mast cells and basophils, and via a complicated cross linking reaction, those cells are led to degranulate and release a variety of chemicals such as histamine, luekotrienes, and prostaglandins, which cause the following reactions illustrated in the figure below (from ‘Harrison’s Principles of Internal Medicine’:

The airway hyper-reactivity and the subsequent inflammatory reactions are done for a good reason. The bronchospasm and mucus hypersecretion limit the exposure of the airways and lungs to the irritant; even the ‘plasma exudation’ is protective. As in any inflammatory response, Elaine Marieb explains:

“Although edema may seem detrimental, it isn’t. The surge of protein-rich fluids into the tissue spaces helps to dilute harmful substances that may be present and delivers important substances such as complement and clotting factors to the interstitial fluid. The clotting factors form a gel-like fibrin mesh that forms a scaffold for permanent repair. This isolates the injured area and prevents the spread of bacteria and other harmful agents into the surrounding tissues…At inflammatory sites where an epithelial barriers has been breached, additional chemicals enter the battle, b-defensins. These broad-spectrum antimicrobial chemicals continuously present in epithelial mucosal cells in small amouns and help maintain the sterile environment of the body’s internal passageways (urinary tract, respiratory bronchi etc). However, when the mucosal surface is abraded or penetrated and the underlying connective tissue becomes inflamed, b-defensin output increases dramatically, helping to control bacterial and fungal colonisation in the exposed area”.

The problem in asthma is that it is inappropriate and excessive. There is no need for it. The situation is especially worse in those with atopic tendencies, and those with eosinophilia and basophilia – the prototype of the two vasculitides, polyarteritis nodosa and Churg-Strauss syndrome. And because of that, asthmatics suffer, and may even die. Surely in that there are signs for people who reflect.


Asthma has troubled the lives of many famous men and women throughout history. I will just pick a few examples of those whose biographical details can actually teach us more about asthma than just the fact that they suffered from it.

Among them are a number of American presidents. I called deep vein thromboses the disease of American presidents, but believe now, having come to know that J. Calvin Coolidge, John F. Kennedy, Theodore Roosevelt, Woodrow Wilson and Martin Van Buren suffered from it, that asthma is an equally valid disease to be described like so. Nevertheless, I will stick to my original designation, because the DVT stories associated with American presidents and vice presidents teach us far more than their asthma attacks.

Nevertheless, the asthma attacks of Martin Van Buren teach us a fair bit about the disease. He was the eighth President of the United States (from 1837 to 1841), and was the first president to be born an American, and the only president ever not to have spoken English as a first language, having grown up speaking Dutch.

Being an asthmatic, Van Buren was prone to very frequent colds, and in summer 1834 was ill for several weeks, and again in late September that year, “with an illness he called "influenza"”. His biographers seem ignorant of the impact asthma could have on a patient, when they say that his frequent coughs and colds were ‘an excuse’. As stated by one biographer, “It has been speculated that the more-frequent-than-usual colds and other ailments he suffered during this period, which often drove him into bed for short periods, may have been an escape”, because “he did not enjoy presiding over the Senate”. This is unjust and unfair on the man.

His biographers regularly mention his frequent dyspepsia, “which he treated with water, soot, and powdered charcoal”. Perhaps this may have been linked with his asthma attacks; acid reflux, it is now established, “has a known association with asthma”.

Towards the end of his life, his asthma (and cardiac failure) predisposed him to his last serious illness, pneumonia, which kept him bedridden during the fall of 1861. He died several months afterwards of “bronchial asthma and heart failure at his Lindenwald estate in Kinderhook at 2:00 a.m. on July 24, 1862”. He is one of the few famous people I know who actually died from the condition, and in remembering him, we will vividly recall a fact that seems unapparent to many people, health care professionals included – that asthma kills.

Another great politician who suffered asthma, that would have no doubt have killed him had he not been killed in battle, was the great Argentine revolutionary, Che Guevara. If you wanted to learn about how asthma can affect the life of a person, Che Guevara is the man you need to know.

He has his first asthma attack at the age of two, and it continued to inflict him throughout his life. As one of his biographers states:

“Early in his childhood, he developed an almost paralyzing degree of asthma that more or less stayed with him for the rest of his life. In fact, it is said that "as one stood next to him, one could hear a wheezing sound coming from his lungs whenever he got too uptight about anything that didn't go his way."”

There can be no doubt about the fact that the continuous stress that he was exposed to throughout his life, and his notorious smoking habits, contributed to his more frequent asthma attacks in later life. There are very few pictures of this great asthmatic when we see him without his Habanos, leading him to be regarded as a ‘Cigar Aficiando’. To him:

“Cigar smoking was not a luxury, but very much a part of the business of revolution, a spiritual complement to lessen the hardships of a life filled with difficulties and dangers…When the doctors tried to prohibit him from smoking, Che negotiated permission to smoke a single cigar a day, and promptly arranged to have an extraordinarily long size rolled for him that he could smoke all day, without violating the agreement.”

Isn’t that hilarious. Che Guevara not only smoked without concern for his asthma, but encouraged others to do, writing in his book, ‘Guerrila Warfare’:

“A customary and extremely important comfort in the life of the guerrilla fighter is a smoke, whether cigars, cigarettes, or pipe tobacco; a smoke in moments of rest is a great friend to the solitary soldier. Pipes are useful, because they permit using to the extreme all tobacco that remains in the butts of cigars and cigarettes at time of scarcity.”

Thus, in learning about Che Guevara’s asthma, we learn of two very important risk factors for asthma attacks – smoking and stress[3].

Nevertheless, despite “suffering from the crippling bouts of asthma that were to afflict him throughout his life, he excelled as an athlete (in his youth). He was an avid rugby union player and earned himself the nickname "Fuser"—a contraction of "El Furibundo" (raging) and his mother's surname "de la Serna"—for his aggressive style of play”. In knowing this, we get to understand that asthmatics can lead absolutely normal lives if they look after their asthma. Needless to say, Che never played rugby in the Bolivian jungles.

His asthma affected his choice of career, and his biographers are unanimously agreed that “Guevara became interested in medicine because of his severe condition of asthma”[4]. It affected his residence and place of living, as “His family had to move to a drier climate when he was a child because of the illness.” It affected his plans to enter the Argentine army to which he applied before applying for medical school, “but was rejected because of his asthma.” Because of his asthma, it took him longer than a normal medical student to graduate from medical school; recalling this fact helps us recall the impact of asthma on school absenteeism. Later on, it affected some of his military plans and judgements. According to his biographer Henry Butterfield Ryan, writing in ‘The Fall of Che Guevara: A Story of Soldiers, Spies, and Diplomats’, towards the end of his life, “Guevara became increasingly ill. He suffered from ever-worsening bouts of asthma, and most of his last offensives were carried out in an attempt to obtain medicine”.

Thus, in the life of Che Guevara we have a fascinating example of how debilitating and dictating a medical condition can be to one’s personal life. I will not mention here reports of his precocious use of prednisolone and his smoking marijuana to help his condition, as some of his biographers state, simply because I believe there is not sufficient evidence for that, and it would be rather anachronistic to state the former.

The final person I would like to discuss here is the great John Locke. Throughout his life he had debilitating attacks, and, “When he became secretary to the newly established Council of Trade and Plantations in 1672, London's fog and smog-polluted air forced him to quit the post in 1675. From 1675 to 1679 he lived in France”. From this biographical piece we learn of another risk factor for asthma attacks – pollution. I have discussed Locke in greater detail in my essay on ‘Philosophy and Medicine’, and will not repeat the discussion here.

Having learnt from the lives of those great men, let us see how asthma can actually affect people, and how it is detected and treated.


Asthma attacks may present with any of WBC:

Breathlessness (intermittent)
Cough (nocturnal cough) / Chest tightness

The attacks tend to occur worst in the evening and early morning; they have ‘morning-dips’; this is attributed to the fact that the airways narrow normally at night, more so in asthmatics, and cortisol levels are also lowest at night. Indeed, the number of nights of disturbed sleep in a week is used to assess the severity of the asthma.

As with any chronic condition, it is important for the patient to give a full picture of his or her illness. This is given by asking the following questions:

When, where, how, what, why was it diagnosed? Too often patient state they are asthmatics simply because they wheeze (and not having had a formal investigation), ignoring the fact that “not all that wheezes is asthma”.
Progression – how has it progressed over the years
Who do you see? What do you do – nebulisers at home? Ask about inhaler technique specifically.
Worst it has ever been? Any admissions to ITU?
How is it now? What is the normal PEFR for the patient? Determine severity by sleep disturbance, impact on ADL and days off work or school. These are objective figures, that can provide a solid basis for observing the effect of treatment on the patient.

Then ask the usual breathlessness questions; in particular note any clear trigger factors, including occupational triggers. The most important things to suspect in someone who has had an acute exacerbation of shortness of breath with asthma are SPINE:

Pneumothorax / PE / Pneumonia
Idiopathic / Infection (URTI)
Non-compliance / NSAIDs and other drugs (e.g. beta blockers)
Exposure to allergen (e.g. House dust mite, dog allergen, cat allergen, pollen, moulds / Exercise


The diagnosis of an acute exacerbation of asthma is made by observation of the following:

May be well or unwell (acute)
JACCOL not relevant, except central cyanosis (severe)
Vital signs extremely important:
RR increased in acute attacks; decreased in life-threatening attacks
PEFR reduced
Saturations reduced
Hypotension in life-threatening attack
Tachycardia in severe; bradycardia in life threatening
Fever in infective exacerbation
GCS reduced in life-threatening; note if able to complete full sentences.

Accessory muscle use and intercostal recession
Deformity (pectus carinatum)
Reduced expansion
Normal TVF unless severe infection
Normal percussion note
Wheezy (silent chest in severe asthma)
PEFR reduced

I find the following mnemonics helpful; in a severe attack patients CANT REALLY TALK PROPERLY:

Cannot talk or feed properly due to breathlessness or cough
RR > 25
Tachycardia > 100 bpm
PEFR < 50 % predicted

While in a life threatening attack, quite simply it is CHEST:

Cyanosis / Confusion / Coma
Silent chest
Threatening PEFR < 33 % predicted

The diagnosis of asthma requires no specialised instruments. It is based on peak flow recording or simple spirometry to look for variability and response to treatment; airway obstruction leads to decreased peak expiratory flow rate (PEFR) and forced expiratory volume in one second (FEV1), althought these may be normal between episodes of bronchospasm. If they are persistently normal, the diagnosis must be in doubt. The diagnosis is certain if:

20% diurnal PEF variation on >3 days per week, in a week of peak flow diary measures
FEV1 > 15% decrease after 6 minutes exercise
FEV1 > 15% (and 200 ml) increase after 2 week trial of oral steroid (30 mg prednisolone once a day)
Bronchodilator reversibility testing FEV1 > 15% (or 200 ml) increase after short-acting agonist therapy (e.g. salbutamol 400 µg by MDI with spacer or 2.5 mg by nebulizer).

It is important to look for the cause of exacerbation:

FBC (FBC & inflammatory markers (raised WCC & CRP in infection); eosinophilia question the diagnosis if high total eosinophil count; consider Churg-Strauss syndrome)
IgE (associated atopy, i.e. positive skin prick tests to common allergens, often with associated allergic rhinitis and eczema)
Aspergillus precipitins (Aspergillus sensitivity, ABPA)

As well as complications, e.g. if saturations <95% do ABGs; CXR (to detect pneumothorax and exclude other diagnoses); low K+ is a complication of salbutamol use in acute exacerbation treatment.


Treatment of asthma is usually divided into that of acute attacks and that of the chronic condition. After the resolution of the former and at every step of the latter, there is a need for a multidisciplinary approach, involving education (e.g. regarding inhaler technique, avoidance of triggers etc) and respiratory nurses, among others.

Treat a severe acute attack with OSHIT, and remember to stick to ABC & MOVE principles:

Oxygen – high flow via reservoir bag
Salbutamol – 5 mg PRN or 2 hourly
Hydrocortisone – 200 mg IV (or prednisolone 40 mg PO if able to swallow)
Ipratropium – 500 mg
Theophylline – aminophylline IV 250 mg over 20 minutes; if patient already on oral theophyllines omit this and urgently check level is therapeutic. Continue at infusion of 1 mg/kg/hour; ECG monitoring is crucial. The alternative is magnesium sulphate 8-16 mmol over 20 minutes

All patients with a life-threatening attack should be discussed with ITU. IM adrenaline should be given if near arrest, whilst waiting for ITU support. As one respiratory consultant put it, “Better to discuss early a patient who does not subsequently need ITU input, than to find you and your patient in difficulty, with no ITU bed.” In addition, patents ought to be discussed with ITU in the following cases:

Worsening PEF despite treatment
Worsening hypoxia
Falling pH
Exhaustion/poor respiratory effort
Respiratory arrest

Only consider discharging the patient after he or she has been put on a reduced b2-agonist dose, off nebulized drugs and on inhalers for 4 hours, with PEFR 75% predicted or best. And ensure the patient has good inhaler technique and a peak flow meter at home, and is able to book an appointment with GP or practice nurse for within 24 hours.

It is interesting that there are a few new trends in the management of an acute attack. Recent BTS guidelines state that ABGs should not be done except if pulse oximetry shows saturations of less than 92%. The oxygen given need not be high flow via non-rebreather; a recent study by Rodrigo et al (2003) showed that it is “better to give low flow oxygen, titrated up to keep oxygen saturations above 92%. A number of asthmatics will start to retain carbon dioxide as they develop hyperinflation and air trapping: limiting the flow of the oxygen minimizes this effect”. Salbutamol need not be nebulised, and need not be 5 mg – 2.5 mg is enough; metered dose inhaler coupled with a spacer is now considered at least as effective, if not more so, because it is faster (1 minute compared to 15 minutes); it “might be best to give 4 puffs, via a spacer every 10 minutes”. All these considerations and recommendations are yet to be established in most UK hospitals; certainly all the hospitals that I have worked in stick to the old regimes.

The chronic management of asthma is as follows, the step number correlating with the number of drugs used in it:

Step 1 – one drug à Salbutamol inhalers as required; 10 puffs per day (2 or more canisters/month) is a marker of poorly controlled disease

Step 2 – two drugs à Add steroid inhalers (e.g. beclomethasone 200-800 mcg/d). Triggers for starting inhaled corticosteroids should be:

An exacerbation in the last 2 years.
Use of beta2-agonist inhaler more than 3 times per week.
Symptomatic of asthma more than 3 times per week.
Waking due to asthma more than once per week.

Step 3 – three drugs à Add on LABA (long-acting beta-2-agonist) (e.g. salmetrol); increase steroids to maximum before going to step 4

Step 4 – four drugs à Add on LT-anatagonist, theophylline or beta-agonist tablet; increase inhaled corticosteroid up to 2000 mcg/d. Refer to specialist.

Step 5 – Add oral steroid tablet and refer to specialist

Regular review should aim to make sure patients are on the appropriate treatment for their disease severity, and are maintained on the lowest possible inhaled steroid dose, so as to reduce side effects of the steroid. Step down treatment if stable for 3 months or more, and step down inhaled steroid by reducing dose by 25-50% at three-monthly intervals. The following table summarizes the stepped care plan for the management oif chronic asthma.

Thus, we conclude our discussion of asthma – a deadly disease, a word which to Arab ears means ‘crisis’. It is important to know that it could be a crisis, and what is more, that it is, in the majority of cases, an avoidable one. This can only be achieved with education of asthmatics, and education of the common man, probably if not certainly, the chief culprit of asthma.
[1] And indeed, it is a mistake to even regard it as ‘reversible airway obstruction’, because of the chronic eosinophilic inflammation. This leads to basement membrane thickening, collagen deposition, and epithelial desquamation and airway remodelling, with smooth muscle hypertrophy and hyperplasia
[2] This is evidenced for by the higher incidence of asthma in those with the eosiniphilic condition, aspergillosis, which is caused by a parasite, Aspergillus fumigatus, which is seen in 1-2% of asthmatics.
[3] Just like we learn of acid reflux as a trigger of asthma from the story of Martin Van Buren.

[4] Though some believe that he entered medical school, “more likely to find a cure for his mother's malignant cancer which she developed at least two years before this decision”.


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