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Childhood Asthma updates in 2024 in Ethi
- 1. Childhood Asthma By: Abeba M.(R2) Moderator: Dr. Abate Yeshidinber, M.D, Ped PCCM
- 2. Outline • Introduction • Epidemiology • Etiology • Pathophysiology • Diagnosis • Management
- 3. Introduction • Asthma is a common, non communicable disease of the lungs affecting both children and adults. • It has a global impact on health care utilization, quality of life, and mortality.
- 4. Introduction • GINA 2022 defines Asthma as heterogeneous disease characterized by chronic air way inflammation • This chronic inflammation heightens the twitchiness of the airways—airways hyperresponsiveness (AHR)— to common provocative exposures • It is defined by history of respiratory sxs that vary overtime & in intensity with variable air flow limitation
- 5. Epidemiology • The heterogeneous nature of the disease makes accurate assessment of prevalence challenging. • Asthma affects 1-18% of the population in different countries • The prevalence of asthma varies by time, place, and population.
- 6. • Worldwide, it is estimated that more than 339 million individuals have asthma, although the prevalence varies among countries • The highest prevalence was in Costa Rica 37.6% while the lowest in the list was Indonesia 2.8% Cont’d…….
- 7. • ISAAC studies indicate that – In 6 to 7 year olds, prevalence of ever having asthma ranged from 3.4% in Africa to 29.2% in Oceania; – In 13 to 14 year olds, prevalence ranged from 5.1% in Northern and Eastern Europe to 22% in Oceania – prevalence rate in Ethiopia was 9.1%, South Africa 20.3%, Kenya 15.8%, Nigeria 13.0%, Morocco 10.4%, Tunisia 11.9% and Algeria 8.7% Cont’d…….
- 8. Cont’d……. • There is an increase in asthma prevalence ~ 50% per decade • Childhood asthma is more prevalent in modern metropolitan locales and more affluent nations, and is strongly linked with other allergic conditions. • Children living in rural areas and farming communities with domestic animals are less likely to experience asthma and allergy.
- 9. • Most countries have an increase in prevalence of asthma in decades before 2000& after that the prevalence continued to increase in countries like Italy & Sweden & reach to plateau in Denmark & Korea • Causes for this change is due to rapidly changing exposures and lifestyles led to asthma developing in susceptible individuals in the latter half of the past century, but the proportion of the population that is susceptible to developing asthma is now reaching capacity Cont’d…….
- 10. • The rate of asthma increases as communities adopt western lifestyles and become urbanized. However, this observation does not fully explain the international patterns of asthma prevalence. • The increase in the prevalence of asthma has been associated with an increase in atopic sensitization and is paralleled by similar increases in other allergic disorders such as eczema and rhinitis Cont’d…….
- 11. Risk factors PRE- AND PERINATAL FACTORS Genetics and familial history Maternal age: Maternal diet during pregnancy Vitamin D, Vitamin E, Vitamin C Polyunsaturated fatty acids: omega-3,EPA, DHA Other vitamins and minerals :antioxidant nutrients, and zinc Maternal asthma Prenatal exposure to maternal smoking Prenatal medication exposure Acetaminophen Acid suppressive medications Antibiotics
- 12. vitamin D intakes and serum levels are associated with lung function in adults& adolescents An inverse association between maternal intakes of vitamin D during pregnancy and early childhood wheezing has been reported in studies from the US and UK vitamin D increase pulmonary defense against respiratory infections &reduce the triggering of asthma exacerbations caused by RTI 1,25(OH)2D3 has a direct anti-proliferative effect on human airway smooth muscle cells and can inhibit the expression of both MMP-9 and ADAM33, suggesting a further beneficial role for vitamin D in the prevention and treatment of asthma administration of vitamin D to glucocorticoid-resistant asthmatic patients can enhance subsequent responsiveness to dexamethasone by restoring the defective IL-10 response to glucocorticoids by CD4+ T cells vitamin D may have alternate modulatory influences on immune function relevant to asthma depending on the time of exposure to it…… the response to vitamin D exposure of naive T cells in the fetus or neonate may be quite different to that of mature T cells Asthma & Vit D
- 13. CHILDHOOD Sex: male Airway hyperresponsiveness Atopy and allergens Influence of microbiome Respiratory infections Medication use in infancy Air pollution Obesity Perinatal factors Pre-eclampsia Prematurity Neonatal jaundice Cesarean delivery Breastfeeding Vitamin D in infancy Risk factors
- 14. • Demographic risk factors – Male gender – Poverty • 80% of all asthmatic patients has onset prior to 6yr of age. • However, of all young children who experience recurrent wheezing, only a minority go on to have persistent asthma in later childhood. Cont’d…….
- 16. Mortality • The Global Burden of Disease (GBD) report estimates that asthma accounts for approximately 420,000 deaths per year(<1 percent of all deaths worldwide). • Avoidable factors (eg, under prescription of inhaled glucocorticoids, insufficient access to emergency medical care or specialist care) still play a part in most asthma deaths in addition to socioeconomic factors and differences in access to medical care
- 17. • The annual death rate from asthma increased from 1982 to 2001 but has since declined • The overall mortality rate was 15.09 per million in 2001 and 9.86 per million in 2017 • According to WHO data published in 2018 Asthma Deaths in Ethiopia reached 4,485 or 0.73% of total deaths. • The age adjusted Death Rate is 8.35 per 100,000 of population Cont’d……
- 18. Etiology combination of environmental and genetic factors in early life shape how the immune system develops and responds to ubiquitous environmental exposures. Respiratory microbes, inhaled allergens, and pollutants that can inflame the lower airways target the disease process to the lungs. Aberrant immune and repair responses to airways injury underlie persistent disease.
- 19. Cont’d…… • Interactions between – host factors (genes, immune maturation, lung development) and – environmental exposures (tobacco smoke, pollution, infection, allergens) and – the timing of these interactions are key in the immunopathogenesis and development of disease manifestation in childhood asthma.
- 20. Pathophysiology • The fundamental pathophysiological features of asthma include – Airway hyperresponsiveness (which can also manifest as reversible airflow obstruction), – inflammation, and – structural changes in the airway wall, collectively termed airway remodeling. • The development of allergic sensitization is also key to the immunopathology of pediatric disease
- 21. Inhaled exposures barrier dysfunction Leaky epithelium allows entry of allergens APCs recognize Ig E Ab synthesized by B cells bind to mast cells release growth factors and mediators symptoms of allergy and asthma.
- 22. Diagnosis • A combination of a – Clinical history of the cardinal symptoms of cough, wheeze, and breathlessness varying over time and – Associated identifiable triggers – Supplemented by measures of airflow obstruction that varies spontaneously or in response to short-acting bronchodilators
- 23. Diagnosis
- 24. Laboratory Findings Pulmonary Function Testing • Spirometry is a helpful objective measure of airflow limitation usually feasible in children >6yr old (with some younger exceptions)
- 25. Spirometry : Airflow limitation Low FEV1 FEV1 /FVC ratio <0.80 Bronchodilator response increase in FEV1 >12% predicted FEV1 >10% Exercise challenge: Worsening in FEV1 ≥15% Daily PEF or FEV1 monitoring day-to-day and/or AM -to-PM variation ≥20%* Exhaled nitric oxide (FeNO) >20 ppb Lung Function Abnormalities in Asthma and Assessment of Airway Inflammation
- 26. Radiology • The findings of chest radiographs (PA and lateral views) in asthma often appear to be normal, aside from subtle and nonspecific findings of hyperinflation and peribronchial thickening. • Chest radiographs can help identify – hallmarks of asthma mimics (aspiration pneumonitis, bronchiolitis obliterans) and – Complications during asthma exacerbations(atelectasis, pneumomediastinum, pneumothorax).
- 27. Other tests • Other tests, such as allergy testing to assess sensitization to inhalant allergens, help with the management and prognosis of asthma. • Acc. To Childhood Asthma Management Program (CAMP) , 88% of patients had inhalant allergen sensitization according to results of allergy skin-prick testing in U.S.
- 28. Types of Childhood Asthma • There are 2 common types of childhood asthma based on different natural courses: (1) recurrent wheezing in early childhood, primarily triggered by common respiratory viral infections, usually resolves during the preschool/lower school years; and (2) chronic asthma associated with allergy that persists into later childhood and often adulthood
- 29. Management Goals of Asthma management • Good control of sxs • Maintain normal activity levels • Minimize future risk – Reduce risk of flare ups – Maintain as close to normal lung function & development – Minimize risk of medication side effects
- 30. Assess • Diagnosis • Sx control • Risk factor • Inhaler adherence • Parent preference Adjust treatment • Medications • Non pharmacological strategies • Tx of modifiable R/F Review response • Medication effectiveness • Side effect Management • Goals of asthma Mnt are achieved through the partnership bln parent/care giver and health care team by:
- 31. 1) Assessment of asthma • Regular assessment and monitoring are based on the concepts of – asthma severity, – asthma control, and – Responsiveness to therapy.
- 32. Asthma severity Daytime symptoms ≤2 days/wk >2days/wk but not Daily Daily Throughout the day Nighttime awakenings: Age 0-4 yr 1-2×/mo 3-4×/mo >1×/wk Age ≥5 yr ≤2×/mo 3-4×/mo >1×/wk but not nightly Often 7×/wk SABA use for symptoms ≤2 days/wk >2 days/wk but not daily, and not > 1× on any day Daily Several times per day Interference with normal activity None Minor limitation Some limitation Extreme limitation
- 33. Asthma severity
- 34. Asthma control • Asthma control means the extent to which the manifestations of asthma are controlled with or without treatment • It has 2 components – Current sx control(status over the past 4wks) – Future risk (previously called impairment & risk)
- 37. Categories of Asthma medications • Controller medications: contain ICS& used to reduce airway inflammation, control sxs & reduce future exacerbations &future decline in lung function • Reliever medications: provided to all patients for relief of break through sxs during asthma exacerbations. Drugs include SABA, low dose ICS formeterol • Add on therapies: considered when patients have persistent sxs &/ exacerbations despite optimized treatment
- 43. 2) Review response & Adjust treatment Assessment at each visit should include: – Asthma sx control – risk factors – Side effects – The need for controller treatment should be assessed Q3-6 months – If rx is step up or down schedule follow up with in 3-6 weeks – For children with seasonal variations in symptoms & exacerbations, provide a written asthma action plan detailing specific signs of worsening of asthma& the medications that should be initiated
- 44. Patient education • Basic explanation about asthma & the factors that influence it • Training about correct inhalation technique • Importance of adherence • Written asthma action plan – Description of how to recognize when sx control is deteriorating – The medications to administer – When & how to obtain medical care
- 45. Patient education Eliminate or Reduce Problematic Environmental Exposures • Environmental tobacco smoke elimination or reduction in home and automobiles • Allergen exposure elimination or reduction in sensitized asthmatic patients: – Animal danders: pets (cats, dogs, rodents, birds) – Pests (mice, rats) – Dust mites
- 46. Patient education Eliminate Other airway irritants: – Cockroaches – Molds – Wood- or coal-burning smoke – Strong chemical odors and – perfumes (e.g., household cleaners) – Dusts
- 47. Treat
- 53. steroid nebulization in acure asthma care in children • The use of ICS in the treatment of acute asthma was studied in four contexts: – In comparison to placebo, – In comparison to systemic corticosteroids, – As add on therapy to systemic steroids with continuation after discharge from the ED, or – As add on therapy to systemic steroids within the ED stay period only.
- 54. Cont’d….. • ICS are superior to placebo especially when given at high doses (>1 mg of budesonide or fluticasone) and to patients with severe exacerbations • GINA guidelines “ICS are effective as part of therapy for asthma exacerbations… and can be as effective as oral corticosteroids at preventing relapses” • A systematic review of 12 trials concluded no benefit of adding inhaled to systemic corticosteroids in reducing the relapse rate of acute asthma.
- 55. Reference • Nelson 21st edition • GINA 2021 update • Manual of pediatric critical care • Keding 9th edition
- 56. Thank you!!!!
Editor's Notes
- In 2011, >10 million children (14% of U.S. children) had ever been diagnosed with asthma, with 70% of this group reporting current asthma. reported asthma prevalence and the prevalence of asthma symptoms showed an increase from the early 1990s until around the end of the 20th century. These include changes over time in diagnostic coding, such as changes in the International Classification of Diseases (ICD) definitions; diagnostic preference, such that wheezing illnesses may or may not be labeled as asthma; increased population awareness leading to more presentations to health care with asthma like symptoms; and systematic bias in questionnaire responses.
- By studying variations of prevalence across the domains of time, place, and person, it is possible to gain insight into the factors influencing asthma in different settings and thereby discover important risk factors for the disease. The prevalence of ever having asthma in 6–11-year-old children in the US increase from 6% in 1973 to 12% in 1988; A similar trend was seen in between the early and late 1970s, in UK, Scandinavia, Israel, New Zealand, and Australia. Two large multicenter studies, the International Study of Asthma and Allergies in Children (ISAAC) and the European Community Respiratory Health Survey (ECRHS) have addressed the issue of variation in methods.
- The reasons for the plateau and potential decrease in prevalence of asthma in some countries remain unclear. It has been hypothesized that the rapidly changing exposures and lifestyles
- The prevalence of asthma in the United States is estimated at 25 million based on data from the National Health Interview Survey [19]. Potential reasons for variation in asthma prevalence have been hypothesized, but none is fully explanatory: ●The rate of asthma increases as communities adopt western lifestyles and become urbanized. However, this observation does not fully explain the international patterns of asthma prevalence. ●The increase in the prevalence of asthma has been associated with an increase in atopic sensitization and is paralleled by similar increases in other allergic disorders such as eczema and rhinitis.
- Genetics and familial history — There are clearly components of the asthma phenotype that appear strongly heritable, although these inherited components do not follow the simple Mendelian pattern, and the specific genes responsible for these inherited components and how they interact with each other and with environmental exposures have yet to be determined. Maternal age — Limited data suggest that increasing maternal age at delivery (age >30 years) is associated with a lower risk of asthma and higher adult lung function in the offspring, compared with younger maternal age…….. increasing maternal age at delivery was associated with a higher forced expiratory volume in one second (FEV1), although this was more consistent among female than male offspring [3]. Asthma decreased with increasing maternal age (odds ratio [OR] 0.85, 95% CI 0.79-0.92) in females, but not males………Young maternal age as a risk factor for the development of asthma was studied in a case-control study of 457 children 3 to 4 years of age with newly diagnosed asthma [2]. Compared with children of mothers who were older than 30 years, children born to mothers younger than 20 years had the highest risk of developing asthma, with an adjusted odds ratio of 3.48. high-dose maternal vitamin D supplementation (eg, 2000 to 4000 IU/day) during pregnancy reduces the risk of early life (up to age three) asthma/wheeze in the offspring Westernized diet has increased the intake of n-6 (or omega-6) polyunsaturated fatty acids (in particular, linoleic acid from plant oils) and decreased intake of n-3 (or omega-3) polyunsaturated fatty acids (particularly, eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] from oily fish). This change may be associated with the increase in the incidence of asthma Other vitamins and minerals — Maternal intakes of the antioxidant nutrients, vitamins E and C and zinc, may modulate the risk for wheezing and asthma in young children, although further study is needed maternal total intake (diet plus supplements) of vitamin E in the highest tertile correlated to reduced development of wheezing symptoms in two year old children, compared with intakes in the lowest tertile (adjusted OR 0. 49) Maternal asthma — Poor maternal asthma control during pregnancy may increase the likelihood of childhood asthma in the offspring based on results from a prospective population-based cohort study, Prenatal exposure to maternal smoking — Prenatal exposure to maternal smoking is a well-established risk factor for childhood asthma, being associated with reduced pulmonary function in the infant and greater likelihood of childhood asthma [41-47]. In addition, smoking during gestation is associated with other adverse pregnancy outcomes, including premature delivery, which is another risk factor for asthma. Prenatal medication exposure — Use of certain medications (eg, acetaminophen, acid suppressive medications, and antibiotics) has been associated with childhood asthma, but often results vary among studies and causality has not been proven. Acetaminophen — Prenatal acetaminophen exposure has been associated with an increase in the risk of early childhood asthma, although results vary among studies Acid suppressive medications — The use of acid suppressive medications during pregnancy has been variably associated with an increased risk of childhood asthma in the offspring Antibiotics — Prenatal antibiotic exposure is associated with a dose-dependent increase in asthma risk depending on the number of courses of antibiotics [58]. However, maternal antibiotic use before and after pregnancy conferred a similar risk, suggesting that the association is not causal.
- large cross-sectional study has shown that vitamin D intakes and serum levels are associated with lung function in adults [9] and similar findings have been reported in adolescents [43]. An inverse association between maternal intakes of vitamin D during pregnancy and early childhood wheezing has been reported in studies from the United States [44] and the United Kingdom These studies raised the possibility that vitamin D may have alternate modulatory influences on immune function relevant to asthma depending on the time of exposure to it. As stated above, vitamin D is associated with skewing the immune response to a Th2 phenotype, with an increase in IL-4 expression. In contrast, others have observed that in human cord blood T cells vitamin D inhibits both IL-12-generated IFN-γ and IL-4 secretion by Th2 cells [46]. Therefore, the response to vitamin D exposure of naive T cells in the fetus or neonate may be quite different to that of mature T cells. the potential for vitamin D to increase pulmonary defence against respiratory infections may, in the same way as in COPD, reduce the triggering of asthma exacerbations caused by RTI [47]. This is supported by the previously mentioned particularly strong negative association between vitamin D status and URTI in individuals with asthma in the Third National Health and Nutrition Examination Survey (NHANES III) study In asthma there is a degree of airway remodelling with an increase in smooth muscle cell numbers. MMP-9(matrix metalloproteinase) is the most relevant enzyme in airway remodelling and is expressed highly in patients with severe irreversible narrowing of the airways. In addition ‘a disintegrin and metalloproteinase-33’ (ADAM33) has been identified as a novel asthma susceptibility gene by genome-wide screening, and is now known to play an important role in airway remodelling. Its level of expression is associated with asthma development and severity and it declines with therapeutic interventions In vitro studies have shown that 1,25(OH)2D3 has a direct anti-proliferative effect on human airway smooth muscle cells and can inhibit the expression of both MMP-9 and ADAM33 [42], suggesting a further beneficial role for vitamin D in the prevention and treatment of asthma. Recently, some evidence has emerged that administration of vitamin D to glucocorticoid-resistant asthmatic patients can enhance subsequent responsiveness to dexamethasone by restoring the defective IL-10 response to glucocorticoids by CD4+ T cells in these individuals [49]. This finding provides encouragement to undertake trials of vitamin D in overcoming glucocorticoid resistance in both asthma and a number of other inflammatory diseases
- Perinatal factors Pre-eclampsia risk factor for childhood asthma (treatment with inhaled glucocorticoids at age 7) in the offspring (adjusted OR 4.01, 95% CI 1.11-14.43), as well as eczema and allergy [59]. Maternal asthma increased the risk of pre-eclampsia. Prematurity — Retrospective studies and meta-analyses have suggested that prematurity is a risk factor for asthma Prematurity was a significant risk factor for both recurrent wheezy bronchitis and asthma in a second cross-sectional study of 1812 primary school children [62]. Neonatal jaundice — The potential role of neonatal jaundice as a risk factor for childhood asthma was examined in a study of 11,321 children in the National Health Insurance Database in Taiwan [84]. After adjustment for confounding factors Mode of delivery — Cesarean delivery may increase the risk of childhood asthma compared with vaginal delivery [67-73]. A population-based cohort study of 1.7 million singleton births found an increased risk of childhood asthma with both planned and emergency cesarean delivery (HR 1.52, 95% CI 1.42-1.62) [71]. One possible explanation is that neonates born by vaginal delivery acquire most of their intestinal flora by exposure to their mother's vaginal fluid during birth; perinatal exposure to microbes on passage through the birth canal then influences early immune modulation. This is an extension of the "hygiene hypothesis" that microbial exposure and infections during early childhood (ie, postnatally) protect against the development of asthma and other allergic disease; however, data in support of this hypothesis are conflicting Breastfeeding — Breastfeeding appears to be associated with a lowered incidence of recurrent wheezing during the first two years of life, possibly reflecting fewer respiratory virus infections. Breastfeeding does not clearly reduce wheezing in later childhood, which is more likely to represent atopic asthma. Vitamin D in infancy: In a trial among 300 premature (28 to 37 weeks) infants of African descent, sustained supplementation (400 IU/day cholecalciferol through six months of age) was compared with placebo (diet-limited supplementation) [85]. The children in the sustained supplementation arm had lower risk for recurrent wheezing by 12 months (RR 0.66, 95%CI 0.47-0.94). While early recurrent wheeze is not asthma, this represents a risk for developing asthma. Sex — Childhood asthma tends to be a predominantly male disease, with the relative male predominance being maximal at puberty [86,87]. After age 20, the prevalence is approximately equal between males and females until age 40, when the disease becomes more common in females Possible explanations include: ●The greater prevalence of atopy (ie, evidence of immunoglobulin E [IgE] sensitization to allergens) in young boys. ●Reduced relative airway size in boys compared with girls [89]. Smaller airway size may also contribute to the increased risk of wheezing after viral respiratory infections in young boys compared with girls. (See "Role of viruses in wheezing and asthma: An overview".) ●Differences in symptom reporting between boys and girls Airway hyperresponsiveness — Abnormal and exaggerated airway responsiveness to noxious stimuli is a central feature in the pathophysiology of asthma, and all patients with asthma have airway hyperresponsiveness (AHR) by definition. AHR is a risk factor for the development of asthma, but not all individuals with AHR will develop asthma Atopy and allergens — Atopy, the genetic predilection to produce specific IgE following exposure to allergens, and sensitization, the development of allergen-specific IgE following exposure, are prerequisites for the development of allergic disease. The association between asthma and other atopic conditions (eg, allergic rhinitis) is well-documented, although sensitized individuals do not necessarily develop allergic disease. Total serum IgE – In a study of 2657 subjects, the prevalence of asthma was closely related to the total serum IgE level, as well as the skin test reactivity The Third National Health and Nutrition Examination Survey (NHANES III), which performed skin testing in 12,106 subjects age 6 to 59 years, found that half of the asthma cases were attributable to atopy (at least one positive skin test) Allergen exposure — A consensus is emerging that indoor allergens (eg, dust mite, animal proteins, cockroach, and fungi) play a significant role in the development of asthma and recurrent wheeze in children Sources of indoor allergens include house dust mites, animal proteins (eg, mouse, cat, and dog allergens), cockroaches, and fungi. Influence of microbiome — Exposure to bacteria and bacterial products may influence the development of allergen sensitization and asthma, although the exact effects appear to depend on a complex interplay of timing of exposure (first year of life versus later in life), location, abundance and diversity of the microbiome, and specific microbial products [120-122]. As an example, early life exposure to allergen and certain bacteria in the environment may lower the risk of asthma [123], while later life exposure to bacteria may increase the risk of asthma. The combination of early-life allergen exposure plus high-level exposure to bacteria in house dust was associated with a further reduction in risk of recurrent wheeze by age three. The mechanism for this protective effect is not known, but changes in gut microflora and related effects on innate immunity are hypothesized. Levels of endotoxin, an inflammatory lipopolysaccharide cell wall constituent of gram-negative bacteria, reflect the degree of microbial exposure. In addition, endotoxin may have a direct immunomodulatory effect. Determinants of endotoxin levels in homes include both indoor sources (eg, pets, pests, humidifiers, kitchen compost bins) and outdoor air. In a nationwide study of 831 representative homes, there was an association between increasing endotoxin levels (greater bacterial exposure) and diagnosed asthma, asthma symptoms in the past year, current use of asthma medications, and wheezing Respiratory infections — Viral and bacterial respiratory infections are well-known triggers of asthma exacerbations in children and adults [125,126]. Whether respiratory infections are a cause of asthma, a marker of susceptibility for asthma, or a protective factor remains unclear Viral respiratory tract infections in infancy, particularly respiratory syncytial virus (RSV) and human rhinovirus (HRV), are predictive of the development of asthma in later childhood to young adulthood, although a causal effect has not been demonstrated Mycoplasma pneumoniae infection was associated with the subsequent development of asthma in a study of 1591 Taiwanese adults and children Medication use in infancy — Epidemiologic studies have found associations between the development of asthma and maternal and infant use of acetaminophen and ibuprofen and also infant intake of antibiotics Air pollution Outdoor — A growing body of evidence suggests that early-life exposure to air pollution increases the risk of pediatric asthma, in addition to the known correlation between levels of air pollution and lung disease in general [154-161]. Results vary among studies, and it is possible that asthma is related to specific pollutants (eg, nitrogen dioxide, carbon monoxide, sulfur dioxide, fine particulate matter), while other respiratory diseases are related to total air pollution. indoor — Contributors to indoor air pollution include products of combustion from gas-fired appliances and indoor fires (eg, NO2, particulates) [166], environmental tobacco smoke [167], and volatile organic compounds (eg, formaldehyde). Obesity — An increased prevalence of asthma is reported among obese children with a dose-dependent effect of body mass index (BMI) on asthma risk
- One of the first rule-based predictive models for early identification of children at high risk of subsequent asthma was the Asthma Predictive Index (API),2 developed in the Tucson Children’s Respiratory Study, which evaluated an unselected general cohort of 1246 infants. Both a “stringent” (Table I) and “loose” index were used to predict asthma at ages 6, 8, 11, and 13 years, based on questionnaire data from ages 2 and 3 years. The positive likelihood ratio (LR+) and negative likelihood ratio (LR−) for asthma diagnosis at age 6 with the use of the stringent index were 7.4 and 0.75, respectively. Based in large part on the results of the Preventing Early Asthma in Kids trial, the National Asthma Education and Prevention Program’s Guidelines for Diagnosis and Management of Asthma from 2007 recommended initiating long-term control therapy in children from birth to 4 years old who are positive for the mAPI to reduce impairment and exacerbation risk.8 The positive posttest probabilities in year 8 and 11 asthma diagnosis were 96% and 89%, respectively
- a study conducted at the capital of Ethiopia, 75.8% of asthmatic patients had uncontrolled asthma. The use of biomass fuel for cooking, longer duration of asthma, incorrect inhalation technique, and asthma exacerbation in the last 12 months was linked with uncontrolled asthma [14]. Similarly, Zewdie at el reported the prevalence of uncontrolled asthma to be as high as 50%. In this study, poor knowledge about asthma, a negative attitude about asthma, moderate asthma, and non-adherence to inhaled corticosteroids were associated with uncontrolled asthma
- Asthma is generally accepted to occur as a consequence of genetic factors interacting with the environment and lifestyle of an individual, perhaps at critical stages of development. Although the cause of childhood asthma has not been determined, a combination of environmental exposures and inherent biologic and genetic susceptibilities has been implicated ETS, environmental tobacco smoke
- The study of asthma genetics is complicated by a number of factors, such as different genes in different individuals leading to the same phenotype, multiple genes acting in one individual to produce the given phenotype, and complex interactions between environmental factors, in addition to the problematic lack of a "gold standard" diagnostic test for asthma. To date, more than 100 genetic loci have been linked to asthma, although relatively few have consistently been linked to asthma in different study cohorts such as :ORMDL3/GSDMB, thymic stromal lymphopoietin (TSLP), and interleukin-33 (IL33), have been identified as important genes for dev’t of asthma
- Altered Pulmonary Immunity in Asthma Inception Inhaled exposures cause barrier dysfunction, which makes the epithelium “leaky” and allows entry of allergens through the airway wall, to be recognized by the pulmonary antigen presenting cells (dendritic cells) for subsequent antigen processing and development of allergic sensitization. Immunoglobulin (Ig)-E antibodies are synthesized by B cells and released into the circulation where they recognize antigen. This is followed by binding to mast cells to release growth factors and mediators results in symptoms of allergy and asthma. In the small airways, airflow is regulated by smooth muscle encircling the airway lumen; bronchoconstriction of these bronchiolar muscular bands restricts or blocks airflow. A cellular inflammatory infiltrate and exudates distinguished by eosinophils, but also including other inflammatory cell types (neutrophils, monocytes, lymphocytes, mast cells, basophils), can fill and obstruct the airways and induce epithelial damage and desquamation into the airways lumen. Helper T lymphocytes and other immune cells that produce proallergic, proinflammatory cytokines (interleukin [IL]-4, IL-5, IL-13), and chemokines (eotaxins) mediate this inflammatory process (see Fig. 169.2 ). Pathogenic immune responses and inflammation may also result from a breach in normal immune regulatory processes (e.g., regulatory T lymphocytes that produce IL-10 and transforming growth factor-β) that dampen effector immunity and inflammation when they are no longer needed. Hypersensitivity or susceptibility to a variety of provocative exposures or triggers (Table 169.3 ) can lead to airways inflammation, AHR, edema, basement membrane thickening, subepithelial collagen deposition, smooth muscle and mucous gland hypertrophy, and mucus hypersecretion—all processes that contribute to airflow obstruction.
- Nitric oxide (NO) is a marker of allergic/eosinophilic inflammation that is easily and quickly measured in exhaled breath. FeNO can be used to distinguish asthma from other airways diseases that are mediated by nonallergic/noneosinophilic inflammation, such as GER, VCD, and cystic fibrosis FeNO can be used to predict response to ICS therapy: • <20 ppb: Unlikely to respond to ICS because eosinophilic inflammation unlikely • 20-35 ppb: Intermediate, may respond to ICS • >35 ppb: Likely to respond to ICS because eosinophilic inflammation is likely
- bronchiolitis obliterans or constrictive bronchiolitis, is a type of bronchiolitis and refers to bronchiolar inflammation with submucosal peribronchial fibrosis associated with luminal stenosis and occlusions hyperlucent lung fields
- School-age children with mild-moderate persistent asthma generally improve as teenagers, with some (about 40%) developing intermittent disease. Milder disease is more likely to remit. Reduced airflow at birth, suggestive of relatively narrow airways; AHR near birth; improves by school age Associated with atopy in early preschool years: • Clinical (e.g., atopic dermatitis in infancy, allergic rhinitis, food allergy) • Biologic (e.g., early inhalant allergen sensitization, increased serum IgE, increased blood eosinophils) • Highest risk for persistence into later childhood and adulthood Lung function abnormalities: • Those with onset before 3 yr of age acquire reduced airflow by school age. • Those with later onset of symptoms, or with later onset of allergen sensitization, are less likely to experience airflow
- impairment consists of an assessment of the patient's recent symptom frequency Risk refers to the likelihood of developing severe asthma exacerbations.
- LRTA----motelukast….zafirlukast Before step-up therapy: review adherence to medications, inhaler technique, environmental control; if alternative treatment option was used in a step, discontinue it and use preferred treatment for that step.
- Use the minimum effective dose of ICS Measure &record child’s height at least yearly The most commonly encountered ICS adverse effects are local: Oral candidiasis (thrush)---- propellant-induced mucosal irritation and local immunosuppression dysphonia (hoarse voice) the result of vocal cord myopathy HFA, hydrofluoroalkane Growth velocity may be lower in the 1st 1-2 years of ICS treatment Poorly controlled asthma, frequent use of oral corticosteroids & pooer nutrition can be the causes
- Risk factors for osteoporosis: presence of other chronic illness(es), medications (corticosteroids, anticonvulsants, heparin, diuretics), low body weight, family history of osteoporosis, significant fracture history disproportionate to trauma, recurrent falls, impaired vision, low dietary calcium and vitamin D intake, and lifestyle factors (decreased physical activity, smoking, alcohol intake).
- Treat Comorbid Conditions Rhinitis Sinusitis Gastroesophageal reflux
- Nebulised ipratropium Bromide: Non-selective muscarinic antagonist and causes short-acting bronchodilation
- recent study found that preemptive use of high dose fluticasone (750 mcg BID) at the onset of an upper respiratory tract infection in children with recurrent virus induced wheezing and continuing it for 10 days, reduced the use of rescue oral corticosteroids. EPR expert panel report state that “high doses of ICS may be considered in the ED, although current evidence is insufficient to permit conclusions about using ICS rather than oral systemic corticosteroids in the ED.”