Bronchial asthma

Prof. Miron Bogdan

Universitatea de Medicina si Farmacie Carol Davila Bucuresti

1. The asthmatic disease

1.1. Definition of Asthma (key words) chronic inflamatory syndrome of the airways Involving several cells (eosinophils, limfocytes, macrophages, mastocytes, epithelial, smooth m cells etc), citokynes and mediators apearing in genetically susceptible individuals Bronchial obstructie reversible partially/complete, spontanously/under treatment BHR to various factors

syndrome

etiopathogenic types
extrinsic (alergic) intrinsic (possibly intricated with COPD) sensitiv to nonsteroid antiinflamators profesional

2.1. Prevalence and mortality

Enhancement of prevalence.
1960-1970

prevalence in nonselected population

USA and in Romania 1,5-2 %

1990

up to present prevalence

USA 4,3 % (1992) Romania 4,5 % (1995)

EPIDEMIOLOGY cont

Factors influencing prevalence

Air

polution (Romania)
intensive polution 12,4 % rural population 3,3 % most incriminated polutants: chemical volatile

age

maximal prevalence beetween 1-17 years and 45-64 years asthmatic children present in 50 % of cases a full remission of de symptoms at puberty

Hypothetical Representation of the Natural History of Asthma

Persistent Asthma Inception Protection No Asthma Asthma Initial Phase Intermittent asthma

Exacerbation No Asthma

Asthma
Heterogeneous condition Lack of well-defined markers for the different disease phenotypes grouped under this common label Most cases of persistent asthma start in early life (first 5 years of life)

Natural history
Many children have asthma-like symptoms during viral infections in the preschool years Most are transient conditions that subside with age Only a minority will have persistent asthma Hard to distinguish who will develop asthma

Respiratory syncytial virus

RSV lower respiratory tract illness was associated with:

significantly

lower measurements of FEV1 an increased risk of wheeze by the age of 6 (risk decreased with age and became not significant by the age of 13)

There was no association between RSV lower respiratory tract illnesses and subsequent atopic status 1999 Aug 14;354(9178):541-5. Stein RT - Lancet.

Phenotypes of wheezing in childhood

Transient wheezing in infancy

Most frequent form of recurrent airway obstruction in infancy (2/3 of infants with asthma-like symptoms) Predisposing factors

Maternal

smoking during pregnancy Lower levels of lung function in the first months of life

Remission factors unknown (growth of the airways/changes of airway tone?)

Development of asthma

Inverse relationship between duration of symptoms and level of lung function in school-age children with asthma1
Sensitization to local aeroallergens is strongly associated with increased risk of asthma in adult life
1.Zeiger RS J. Allergy Clin. Immunol. 1999;103:376-87.

Development of asthma

Asthma between school years and mid adult life is associated with:
Sensitization

to local aeroallergens Elevated total circulating IgE Both1

Hypothesis - Sensitization to specific allergens (early life) is the cause of asthma (IgE specific)
1. Burrows B N Engl J Med 1989;320:271-7.

Development of asthma
Children with skin-test negative to Alternaria develop asthma-like symptoms in the first year of life Children with skin-test positive to Alternaria have peak incidence of asthmalike symptoms at age 2-3 In both groups inception of symptoms before age 3 Non-atopic asthma develop earlier than Halonen M Am. J. Respir. Crit Care Med 1999;160:564-70 atopic asthma (different mechanisms)

Development of asthma

Increasing prevalence of pediatric asthma

Western environmental pro-asthmatic factors

Von Mutius E J Allergy Clin Immunol. 2002 Jun;109(6 Suppl):S525-32

Development of asthma

Studies performed in low exposure to house dust mites areas prevalence of asthma is similar or higher than in areas with high exposure1 N. Sweden (low indoor exposure to dust mites/molds ) similar prevalence of schoolage asthma with S. Sweden (high exposure) 2 Skin-negative children with asthma have higher IgE than non-asthmatic2
1. Halonen M Am. J. Respir. Crit Care Med 1998;155(4):1356-61 2. Perzanowski MS J .Allergy Clin. Immunol. 1999;23:812-20

Outcome of asthma in adult life

Asthma remits in early adulthood in a large proportion of patients (~50%) Most children with severe symptoms will develop severe symptoms in adulthood Most children with mild symptoms will develop mild/no symptoms in adulthood Allergic symptoms (rhinitis, eczema) are associated with persistence of asthma into 1. J. 1969:4:321-5 adult lifeWilliams H Br Med.Med.2000;94:454-65 2. Kjellman B Respir.

Outcome of asthma in adult life

Factors associated with relapses of asthma in adulthood with symptoms remitted during teenage period unknown (appears to be independent of allergies and smoking)
1

Smoking2 produces an excessive rate of decline of FEV1 (overlap asthma COPD)

1. Strachan DP Br. Med. J.1996;312:1195-9 2. Camilli AE Am. J. Respir. Crit. Care Med.1987;135:794-9

MORTALITY
UK, 1982 aparent higher prevalence of deaths among asthmatics by comparison with 1970 (>2 folds) ANALYSIS of the deceased: 86 % of the cases could be prevented!!!

current physicians: were not able to appeciate the severity of the cases pacients noninformed upon their disease Insuficient use of antiinflammatory drugs

MORTALITY cont
Asthmatics with life threatening forms have to be identified and actively treated and medically surveyed 1998 for first time the mortalitaty in BA is comparable with the general population

2.3. Social impact

USA there are 15 millions asthmatics In Romania there are 1 million asthmatics! Major cost of drugs Major cost of frequent hospitalizations Major social economic cost by losing working days

Pathology: chronic inflammation of the airways

Postmortem studies ( asthmatic deceased ) Ellis, 1906
Macro: distended lungs , circumscribed atelectasia by dopuri de mucous plugs that were obstructing subsegmentary bronchi. Micro: important thikening of the bronchial wall (edema, glandular hiperplasia, thikening of the basal membrane, thikening of the smooth muscle cell layer, important cellulear inflammatory infiltration especially with eosinophils and lymphocytes); extensive necrosis of the bronchial epithelium with mucosal uncovering.

Chronic inflammation of the airways

Studies in vivo: made possible by the introduction of Fibrobronchoscopy (1980-) bronchial biopsy: microscopic features met in
postmortem studies were found even in mild and medium severe forms of asthma and even during clinical remission

broncho-alveolar lavage (BAL): a method able

to identify and characterize the cells and the mediators involved in asthmatic inflammation

Imagine - ingrosarea mb. bazale 1

Imagine-ingrosarea mb. bazale 2

Imagine-distributie tridimensionala fmn

Imagine-hipertrofie/hiperplazie fmn

Asthmatic inflammation: involved cells

Bronchial asthma is a disease determined by an immune pathological mechanism, IgE mediated (group l Gell - Coombs) All the cells involved in the chain of the immune reactions will be also active in bronchial asthma

Cellular mechanisms in BA Mecanisme celulare in AB

Histamine, LT, 5OHT MC Early reaction

Atg
LT LTh2

LB IL4 IL5

Eoz

Late LT,PAF proteine cationice reaction

CHRONIC INFLAMMATION

CELULE PROINFLAMATORII SI CELULE TINTA

Inflammatory cells
MastC LT Mf MEDIATORs SI CYTOKINES Epithelium Eoz

Target cells

Fibroblast Smooth muscle Vascular endothelium

Relationships: cells mediators - obstruction

ACTIVATED CELLS MastC Mf Eoz Epithelium LTh2 Thrombocytes Smooth muscle PMN

Bronhoconstriction MEDIATORS SOUP hystamine leucotrienes peptides cytokines growth factors Vascular leakage Bronchial hypersecr.

Bronchial hypereact.

CONCLUSIONS
1.
2.

3. 4.

Chronic inflammation: eosynophils Different inflamatory profile as in COPD, Bronchiectasis, Infectious bronchitis Maximal therapeutic effect: corticosteroids Antibiotherapy: not indicated

BRONCHIAL REMODELING BRONCHIAL HIPERREACTIVITY

Bronchial asthmatic remodeling: morphologic global consequences of chronic inflammation

The physiopathological consequence of br. remodeling: br. hyperreactivity

BRONCHIAL HIPERREACTIVITY

Definition: the ability of the bronchi to decrease their diameter to stimuli that are usually indifferent Types of stimuli: 1. Physical: Low temperature, effort 2. Chemical: NO2, SO2, ozone, chlorine, NH3 3. Infectious: respiratory viruses 4. Air polutants: smoke, gases, volatiles 5. Vagal reflexes, psychological negative stimuli

Bronchial remoddeling - BHR

NORMAL ASTM

Bronchial progressive fibrosis late asthma evolution

Progressive fibrosis of the extra cellular matrix of bronchial wall Determines a partially irreversible chronic obstructive sindrome

Relation INFLAMMATIONBHR-SYMPTOMS
Alergens, viral infections Genetic susceptibility Air pollution, irritants -atopia

Eosinophilic chronic inflammation

Hiperreactivitate bronsica

Asthmatic symptoms

Triggers

CONCLUSIONS
Chronic inflammation induces hyperreactivity Severe hyperreactivity induces symptoms Controlling symptoms means diminishing inflammation Viral infections can trigger asthmatic exacerbations (but asthma is not an infection!)

Risk factors in asthma

RF for appearance of the disease:

predisposition:

atopy causal: alergens, non-steroid antiinflamatory drugs, work related molecules adjuvant: respiratory infections, air polution, smoking (active and second hand)

RF for enhancing the disease: triggers

Risk factors: significance

NOT SCHOLASTIC AB classification alergic/extrinsic, professional, NSAI related, intrinsic, etc.

BUT PRAGMATICAL Systematic search for a causal factor in the patients enviroment Build up efficient therapeutic strategies

Allergens

Indoor:
mytes

(main cause for sensitisation) animal allergens (cats high amount of sensitisation, dogs, rodents) cockroaches (main cause in some areas) fungi

Outdoor:
pollens fungi

(trees, grass, and ??)

Asthma diagnosis

Asthmatic symptoms Physical exam signs of obstruction/hyperinflation Variable obstructive syndrome confirms the diagnosis
Atopy Family history Identifying of causal factors and triggers (interview and prick tests)

Asthmatic symptoms

Dyspneea
Usually

dominant, rarely absent >/< paroxystical expiratory

Wheezing
Usually

associated with dyspneea relatively specific

Other symptoms

Cough
rarely

dominant, usualy associated to dyspneea Dry, non productive, (purulent sputum could be induced by excessive eosynophils) sometimes severe

Chest tightness
Associated

with dyspneea

Asthmatic symptoms

variable:
Associated

with trigger factors Spontaneously or therapeutically improved

Nocturnal predominance
or

As a consequence of a trigger (effort)

Clinical behaviour of asthmatics

Asthmatic crisis
Asthmatic exacerbation Continuous symptoms Coughing asthma

Physical examination

Respiratory rate: normal or mildly enhanced Signs of bronchial obstruction:

Prolonged

exhalation (inclusiv auscultator) Diffuse weezes Diffuse diminishing of breath sounds (severe obstruction)

Hyperinflation signs: increased thoracic diameters (anterior and posterior)

May not be present normal physical exam doesnt exclude asthma

Symptoms + physical signs

= consultation time
semne simptome

Variable obstructive syndrome

Pulmonary function tests

Spirometry:
FEV1

(Forced Expiratory Volume in the first second) VC (Vital Capacity) calculating VEMS/CV% ration (bronchial permeability index)

Peak-flow-metry
PEF

(Peak Expiratory Flow)

Measuring PEF (peakflow-metry)

Simple Available and cheap Relatively accurate,

depends

by: Patient effort (ideally maximum) Reliability of the technique Enhanced by repeating the measurement

ideal for measuring pulmonary function

In the GP office At home by the patient

Variable Obstructive Syndrome

- PEF assessed

Improvement of PEF by more than 15% at 15-20 (max. 30) minute after bronchodilation (a short acting 2 agonist) Variable PEF more than 20% morning/evening and taking a bronchodilator (or more than 10% without taking a bronchodilator) Reduction of PEF with more than 15% at 5-10 minutes after an effort (running) of 6 minutes

PEF chart
600 500 400 300 200 100 0 1a 1p 2a 2p 3a 3p 4a 4p 5a 5p 6a 6p 7a 7p 1 2 3

PEF vesperal - PEF matinal variabilitate zilnica = (PEF vesperal + PEF matinal)

Spirometry
FEV1, VC si FEV1/VC = most validated functional respiratory parameters Necessitates a trained staff Relatively expensive and less achievable Very important for recomandabila pentru diagnosis and for follow up

Spirometry
Obstructive syndrome:
FEV1

< 80% of predicted VEMS/CVF < 70%

Reversible after a short acting 2 agonist

Improvement

of FEV1 by more than 15% vs the initial value

Spirometry
Ref. CV (VC) VEMS (FEV1) 4,8 l 4,0 l Pre Post Dif.

4,3 l 89,6% 4,7 l 97,9% 9,3% 3,0 l 75,0% 3,9 l 97,5% 30,0% 84,8%

VEMS/ 83,3% 69,8% CV

5. Asthma DIFFERENTIAL diagnosis

1. Bronchoconstriction after viral infectious events 2. Reactive airway disease (RADS) 3. COPD 4. Left ventricle failure 5. Sleep Snorring Apnea (SAS) 6. Benign tracheal tumors 7. Diskynetic vocal cords 8. Anxiety (Tachipnea)

Terapia astmului bronsic

1. Educatia pacientului 2. Evictia alergenilor 3. Medicamente folosite 4. Strategia tratamentului 5. Exacerbarea terapie 6. Astmul amenintator de viata

Medicaia antiastmatic

Antiastmatice

Controller (control) Reliever (usurare)

Antiastmatice-controller
Corticoizi inhalatorii Corticoizi sistemici Teofiline retard Beta 2 agoniti de lung durat Anti-leucotriene Anti-IgE

Antiastmatice-reliever

Beta 2 agoniti de scurt durat

Beta 2 agoniti orali de scurt durat

Corticoizi sistemici Anticolinergice Teofiline cu durat scurt de aciune i.v.

Planul prezentrii clasei de medicamente

Prezentarea substanei Efectele antiastmatice Tolerana-cale de administrare,doze Efectele secundare -locale i sistemice Strategia utilizrii n tratamentul antiastmatic

Medicaia controller
Medicaie zilnic Tratament de durat,controlul la distan al bolii Agenii antiinflamatori,agenii antialergicicei mai eficaci Msur de profilaxie secundar Nu n criz

Medicaia -reliever

Acioneaz rapid
Administrate la nevoie

Terapia de baz pentru cuparea crizei Nu au efecte de lung durat

Corticoizii inhalatoricontroller
Beclometazon dipropionat Budesonid Triamcinolon acetonid Fluticasone propionat Flunisolide

Corticoizii inhalatoricontroller

Cei mai puternici antiinflamatori

Acioneaz pe celule proinflamatorii,mediatori,etc. Crete rspunsul la beta agonist

Corticoizii inhalatoricontroller
Calea de administrare-inhalatorie Administrare pe calea aerosol dozatoarelor sau sub form de pulbere cu inhaler tip Turbuhaler,Discushaler,etc Toleran foarte bun-anxietate nemotivat

Corticoizii inhalatoricontroller
Dozele(g) Beclometazon diprop.-200-1000 Budesonid-200-800 Flunisolide-500-2000 Fluticasone prop.-100-650 Triamcinolone acet.-400-2000

Corticoizii inhalatoricontroller
Efecte sistemice: foarte rare, legate de absorbia tract gastro-intest. Efecte sistemice excepionale-suprarenale, os,oculare Medicaie de elecie n astmul bronic

Corticoizii sistemicicontroller
Aciune antiinflamatorie puternic Mecanismele de aciune simi- lare cu ale corticoizilor topici

Efectele secundare mult mai evidente

Corticoizii sistemicicontroller
Indicaiile: exacerbrile de astm tratamentul scurt de oc -con trolul rapid al astmului cronic declinul gradual al unui astm cu tratament corect tratamentul pe termen lung al astmului cronic n stadiul IV,status astmaticus

Corticoizii sistemicicontroller
Doze: 0,5-1 mg per kgcorp folosire doze minime schimbare doze gradual i lent cretere doze la infecii severe,traume,intervenii chirurgicale,tratament dentar tratament zilnic sau alternativ administrare matinal

Corticoizii sistemicicontroller
Efecte secundare: folosire ndelungat osteoporoz,fracturi spontane HTA,diabet zaharat,obezitate, cataract,subiere piele, simpto me gastrointestinale,tulburri mentale(euforie,depresii,manii),Cushing,sl biciune muscular,oprire cretere, Supresia suprarenalei

Teofiline retardcontroller
Cele mai importante metilxantine utilizate n astm Efect antiinflamator mai mic i imunomodulator la doze mai mari Efect bronhodilatator la dozele obinuite Efect pe hiperreactivitatea bronic

Teofiline retardcontroller
Administrare-oral sau parenteral Forme de prezentare-tablete de la 100-600 mg Recomandarea de familiarizare cu un produs i a nu se ncerca trecerea de la un produs la altul

Teofiline retardcontroller

Inhib fosfodiesterazele
Inhib reacia imediat i tardi v Relaxeaz musculatura neted, stimuleaz contracia diafrag mului

Teofiline retardcontroller
Concentraia seric-5-15g/ml Doza toxic apropiat de cea terapeutic Efecte secundare n trepte: -grea,vom,tahiaritmii,agitaie -cefalee,hiperxcitabilitate neuro muscular,,insomnii,gastralgii, diurez crescut,tulburri de comportament -convulsii

Teofiline retardcontroller
Dozare riguroas cretere treptat a dozelor scderea lor cu 25% din doza dac apar efecte adverse monitorizare clinic,PEF ,teofili nemiei de preferat administrrile unice sau de dou ori pe zi-compliana

Beta 2 agonitii de lung duratcontroller

Salmeterol
Formoterol

Beta 2 agonitii de lung duratcontroller

Modaliti de administrare inhalatorie-aerosol dozator,nebulizare oral-tablete sau sirop Durata de aciune: 12 h Forme de prezentare:aerosol dozatoare,tablete

Beta 2 agonitii de lung duratcontroller

Mecanisme de aciune relaxeaz musculatura neted inhib rspunsul imediat i tardiv scade permeabilitatea vascular efect antiinflamator mai mic,crete clearance mucociliar moduleaz eliberarea de mediatori din bazofil,mastocit

Beta 2 agonitii de lung duratcontroller

Administrare 1-2 pufuri la 12 h Trebuie nsoii de antiinflamat oare Nu se administreaz n criz Tabletele -dac nu accept sau nu administreaz corect aerosolii

Anti-leucotriene-controller

Ageni folosii relativ recent

Montelukast Zafirlukast

Anti-leucotriene -controller
Aciune: inhib receptori leucotrienelor inhib bronhoconstricia reduc rspunsul indus de aler -gen, efort,aer rece i aspirin efecte antiinflamatoare uoare reduc inflamaia eozinofilic

Anti-leucotriene -controller
Form oral Dozare Administrare Montelukast-o tablet 10 mg pe zi Zafirlukast-2 tablete

Anti-leucotriene -controller
Toleran foarte bun Efecte adverse uoare disfuncii hepatice cefalee,dureri abdominale

Anti-leucotriene -controller
Utlizare clinic: astmul uor i moderat pe termen lung pentru reducerea simptomelor,necesar de beta 2 agoniti, funciei pulm. Pacienii care nu sunt controlai cu corticoizi inhalatori Astm sever,la aspirin,la efort

Beta 2 agoniti de scurt duratreliever

Salbutamol(albuterol) Fenoterol Terbutalina,etc

Beta 2 agoniti de scurt duratreliever

Sub form de aerosol dozatoare,turbohaler Tablete(slow-release),siropSalbutamol,Terbutalina Nebulizare Pudr Fiole cu administrare s.c. (terbutalina)

Beta 2 agoniti de scurt duratreliever

Doze: astmul stabil doze minime 100-200g astmul cu obstrucii severe-4000 g-pn la 20 de pufuri relaie doz-rspuns administrare la nevoie tendina de supradozare

Beta 2 agoniti de scurt duratreliever

Toleran foarte bun-poate induce tahifilaxie Contraindicate:tulburri de ritm grave Efecte adverse: tremurturi, tahicardie,palpitaii,agitaie Hipokaliemie Hipoxemie(vasodilataie) Agravare astm la doze foarte mari

Beta 2 agoniti de scurt duratreliever

Beta 2 agonitii orali au efecte adverse ca de ex.stimularea cardiovascular,tremurturile,hipokaliemia i iritabilitatea mai semnificative ca la alte terapii Indicai la bolnavii care nu sunt capabili s utilizeze medicaia inhalatorie

Beta 2 agoniti de scurt duratreliever

Anterior unor stimuli declanatoriefort,alergen nlturare imediat simptome Marker de severitate(posibil cretere morbiditate, mortalitate) i.v-astmul sever-pericol deces

Beta 2 agoniti de scurt duratreliever

Concluzii: nu exist incompatibilitate cu beta 2 agonitii de lung durat anxietatea indus pacienilor nefondat comparativ cu efectele corticoterapiei parenterale

Corticoizi sistemici-i.v.reliever

Hemisuccinat de hidrocortizon
Metilprednisolon

Corticoizi sistemici-reliever
Aciune-efectele corticoterapiei sistemice Administrare i.v. Doze-200 mg la 4-6 h-hemisucci nat -100 mg la 6 h metilprednisolon

Corticoizi sistemici-reliever
Efecte adverse-vezi corticoizi orali Utilizare: astmul sever-terapia bronhodilatatorie inadecvat exacerbarea de astm ,astm amenintor de via

Corticoizi sistemici -reliever

Concluzii este vorba de o terapie utilizat n excesnemotivat durata utilizrii i reducerea dozelor depinde de rspunsul pacientului i de trecutul su se poate trece ulterior pe corticoterapie oral sau inhalatorie

Anticolinergice-reliever
Ipratropium bromid(20/40/g/puf) Oxitropium bromid(100 g/puf)

Asocieri-cu fenoterol,

Anticolinergice-reliever
Antagonist de receptori muscarinici Inhib bronhoconstricia reflex Efect mic antiinflamator,pe mas tocite,exudarea vascular, mediatori

Anticolinergice-reliever
Administrare n aerosoli, nebulizare Doze: 1-2 pufuri la nevoie pn la 8 pufuri de 20g-0,5 mg Administrare regulat sau la nevoie Relaie doz-rspuns

Anticolinergice-reliever
Toleran foarte bun,fr fenomene de tahifilaxie Efecte adverse:uscciunea gurii,disurie,constipaie cretere vscozitate sput gust amrui glaucom bronhoconstricie paradoxal(nebulizare)

Anticolinergice-reliever
Utilizare:astm nocturn n astmul sever ca alternativ pentru beta 2 agoniti La pacienii cu doze mari corticoizi inhalatori-efect adiional La btrni cu probleme diagnostic diferenial cu BPOC

Anticolinergice--reliever
Concluzii: astmul bronic nu reprezint indicaia de elecie avantajul uneori al asocierii cu beta 2 agoniti mai puin eficace n astmul cronic,utilizabil n astmul acut

Teofiline de scurt durat i.v.reliever

Aminofilina

Teofiline de scurt durat i.v.reliever

Mecanisme de aciune similare cu teofilinele Efectul se instaleaz mult mai rapid Bronhodilatator mai slab dect beta 2 agoniti Fluctuaii ale concentraiei serice

Teofiline de scurt durat reliever

Administrare-i.v.,oral? Doze de ncrcare 7mg/kg pn la 250 mg n 20 min meninere 0,5-1 mg/kg Se poate asocia cu teofiline retard dar atenie la monitorizarea teofilinemiei i a reaciilor adverse

Teofiline de scurt durat i.v.reliever

Toleran bun Reacii minore -tahicardie ,tremurturi,hipotensiune la injecii rapide Efecte adverse similare cu teofilinele Supradozare-grea,vom,aritmii ,convulsii

Teofiline de scurt durat i.v.reliever

Indicaii n caz de inaccesabilitate beta 2 agoniti pretratament la astmul la efort controversate n exacerbarea de astm

Teofiline de scurt durat reliever

Concluzii adugarea lor poate crete mortalitatea nu se preteaz la tratament cronic poate susine funcia ntre prizele de beta2 agoniti crete efectele secundare adugat beta 2 agonitilor se exagereaz utilizarea i sunt subdozate

Terapia ideal-I
Controlul i nu vindecarea astmului
Simptome minime(nocturne) Minimalizarea exacerbri Diminuare solicitri servicii de urgen

Terapia ideal-II
Minim necesar de medicaie (beta 2 agoniti) Fr limitarea activitilor,efort Variaie PEF circadian sub 20% Normalizare PEF Minimalizarea efecte adverse

10. Trepte de severitate

CRITERIILE de definire a treptelor de severitate

anterior tratamentului: Simptome diurne Simptome nocturne PEF

Pozitivitatea unui singur criteriu corespunzator unei trepte este suficient pentru a plasa pacientul in respectiva treapta

10. Trepte de severitate /cont Treapta 1: Astm intermitent

Simptome diurne: - <1episod/saptamina Simptome nocturne: - 2/luna Asimptomatic si cu PEF normal intre crize
PEF: -variabilitate <20% - >80% din valoarea standard

10. Trepte de severitate /cont Treapta 2:Astm usor persistent

Simptome diurne: - 1episod/saptamina dar <1episod/zi Simptome nocturne: - >2/luna PEF: -variabilitate 20-30% - >80% din valoarea standard

10. Trepte de severitate /cont Treapta 3: Astm moderat persistent

Simptome diurne: zilnice -utilizare zilnica de 2 agonisti -crizele interfera activitatea zilnica
Simptome nocturne: - >1/saptamina PEF: -variabilitate >30% - 60-80% din valoarea standard

10. Trepte de severitate /cont Treapta 4: Astm sever persistent

Simptome diurne: continue -limiteaza activitatea fizica Simptome nocturne: -frecvente PEF: -variabilitate >30%
- 60% din valoarea standard

13.Tratamentul in trepte in functie de gradul de severitate

Treapta 1: Astm intermitent

Tratament de control:
-nu este necesar

Tratament simptomatic: - 2 agonisti inhalatori <1/saptamina

- intensitatea tratamentului depinde de severitatea crizei - 2 agonist sau cromoglicat inainte de efort sau expunere la alergeni

13.Tratamentul in trepte in functie de gradul de severitate

Treapta 2: Astm usor persistent

Tratament de control:
-corticosteroizi inhalatori (CSI) 200-500 g/zi sau cromoglicat sau nedocromil sau teofilina retard sau antileucotriene

- se poate creste doza de CSI la 800 g/zi sau

se poate asocia 2 agonist cu durata lunga de actiune (inhalator, tablete, sirop) sau teofilina retard (in special pentru simptomele nocturne)

Tratament simptomatic:

- 2 agonist inhalator cu durata scurta de actiune 3-4ori/zi

13.Tratamentul in trepte in functie de gradul de severitate

Tratament de control:

Treapta 3:Astm moderat persistent

-corticosteroizi inhalatori 800-2000 g/zi SI - 2 agonist cu durata lunga de actiune (inhalator, tablete, sirop) sau teofilina retard (in special pentru simptomele nocturne) sau antileucotriene

Tratament simptomatic:

- 2 agonist inhalator cu durata scurta de actiune 3-4ori/zi

13.Tratamentul in trepte in functie de gradul de severitate

Treapta 4: Astm sever persistent

Tratament de control:
-corticosteroizi inhalatori 800-2000 g/zi sau mai mult, ASOCIAT CU - 2 agonist cu durata lunga de actiune (inhalator, tablete, sirop) sau teofilina retard UNEORI ASOCIAT CU -corticosteroizi p.o. (tablete, sirop) pe termen lung

Tratament simptomatic:
- 2 agonist inhalator cu durata scurta de actiune in functie de simptomatologie

13.Tratamentul in trepte in functie de gradul de severitate

Criteriile schimbarii de treapta terapeutica

Treapta in jos
revizuire a tratamentului la 3-6 luni daca se obtine controlul simptomatologiei >3 luni se poate incerca o reducere a tratamentului (pe o treapta inferioara)

Treapta in sus
daca nu se obtine controlul simptomatologiei inainte de toate: revizuiti corectitudinea tehnicii administrarii medicatiei de catre pacient,complianta la tratament, controlul factorilor de mediu declansatori ai crizelor

Astmul amenintor de via/AAV-urgena imediat

Identificare
Definiie
Patogenie

PEF
Clinic
Criterii

de internare

Forme clinice potential evolutive catre astm amenintator de viata (AAV)

Astm sever Astm fragil (brittle) Astm cronic cu evoluie dificil

Definiie astm sever

Atacuri recurente Simptomatologie bogat Interferen cu somnul Rspuns inadecvat la beta 2 adrenergice

Definiie-astmul fragil
Fr probleme n cursul zilei dar cu crize severe n cursul nopii Frecvente vizite n clinic Frecvente cure de corticoizi Frecvente reacii adverse la acetia

Definiie-astm cronic dificil

Determin rar exacerbri severe Simptomatologie nocturna-altereaza structura somnului Interfer cu tolerana la efort, capacitatea de a lucra, studia sau a se juca(copii) Adesea probleme de complian Dificil din punct de vedere al pacientului

Factori de risc pentru astm amenintator de viata (AAV)

Purttor al unui risc crescut de atacuri severe sau deces Episoade de insuficien respiratorie intubaie Episod de acidoz respiratorie 2 sau mai multe internri-sub corticoizi orali i topici episoade de pneumomediastin sau pneumotorax

Modul de instalare al atacurilor AAV

Instalare foarte rapid

Altele cu deteriorare lent clinic i funcional

Patogenia AAV

Ocluzia cu secreii vscoase a cilor aeriene

Remodelare bronsica severa Bronhospasm sever persistent

Definire funcional
Se poate folosi PEF sau VEMS Atenie chiar un inspir profund poate agrava bronhoconstricia PEF la 30-50% din prezis PEF sub 120 sau FEV1 sub 1litru PEF sub 33%-risc deces-intubaie

Rspunsul la tratament
Cel mai important indicator predictiv Pozitiv = la 30 de minute de la tratament ameliorare simptomatologic Negativ = la 2 h modificri minime ale PEFR spitalizare gazometria (spital)

Markeri de severitate
Pa CO2 normal(36-45 mmHg) sau crescut Hipoxie sever: Pa O2 sub 60 mmHg pH sczut Prezenta unui marker este suficienta pentru a confirma severitatea

Criterii de admitere n spital

-spitalizri anterioare -dependena de corticoizi -folosirea excesiv sau depen dena de aerosol-dozatoare -agravare sau prelungire simptomatologie

Criterii de admitere n spital

ntoarcerea

la camera de gard dup tratamentul iniial semne de severitate-puls pa radoxal mai mare de 18 mmHg,folosirea muschi accesorii -absenta rspuns la terapie n urmtoarele 2-6h

Criterii de admitere n terapie intensiva

Indicaii definitive -semne de insuficien respira torie: cianoz, PaO2 sub 55 mm Hg,diaforez,hipercapnie,altera re status mental, fatigabilitate. -complicaii pulmonare secunda re:pneumonia, condensarea pul monar, pneumotorax, pneumo mediastin

Adresabilitatea la spital a cazurilor

Depinde

de : -experiena i gradul de expertizare al medicului de familie -aranjamentele locale stabilite cu medicul pneumolog

Pacienii potenial candidai la internare

Cei care au nevoie de corticoizi orali mai mult de 2-3 ori per an Cei cu necesar de corticoizi to pici peste 800 mcg beclometa zon Cei la care se consider necesa r utilizarea cronic de corti coizi orali

Astmul sever n practica general

Astmul necontrolat -vorbire normal -pulsul sub 110 bti/ min -respiraia sub25/min -PEF peste 50% din cel prezis tratat la domiciliu dar rspunsul la tratament trebuie confirmat nainte de plecare

Astmul sever n practica general

Astmul sever acut -nu poate s ncheie frazele -pulsul > 110 bti/min -respiratia 25/min PEF 50% din cel prezis se ia n considerare serios posibilitatea internrii dac are mai mult de una din caracteris ticile amintite

Astmul sever n practica general

Astmul amenintator de viata -stetacustic-torace linitit -cianoz -bradicardie ,hipotensiune, puls paradoxal -epuizare,confuziv,comatos -PEF 33% din valoarea prezis internare imediat

Semne avertizante ale severitii

Dispnee n repaus Tahicardie Pulsul paradoxal PEF sub 120 l per min Anomalii gazometrice

15. STABILIREA UNUI PARTENERIAT CU PACIENTUL

Capacitatea de a monitoriza tratamentul pe termen lung

15. PARTENERIAT
Medicul ce trateaza un Astmatic nu se angajeaza la un ACT MEDICAL IZOLAT O boala cronica are nevoie de o ASISTENTA MEDICALA DE PERSPECTIVA Medicul de Familie poate reprezenta Partenerul/Manager al pacientului Astmatic

15. PARTENERIAT cont

Primul consult: precizarea diagnosticului

stabilirea

unei COMUNICARI optime cu

pacientul EVALUAREA PROFILULUI PSIHOLOGIC grad de instructie: nivel de comunicare ce interes are de a cunoaste date despre boala sa? atitudinea sa fata de boala:

Depresie?

Anxietate?

EDUCAREA

PACIENTULUI

15. PARTENERIAT cont

EDUCAREA PACIENTULUI
Astmul

este o boala cronica DAR cu tratament adecvat viata Astmaticului este o VIATA NORMALA Tratamentul trebuie inteles Tratamentul trebuie urmat pe termen lung Trebuie pastrata legatura cu Medicul Scopul actiunii medicului este dobandirea unei AUTONOMII de catre pacient

15. PARTENERIAT cont

Astmaticul trebuie sa invete:

sa

isi administreze medicamentele corect sa inteleaga diferenta intre medicament reliever si controler sa evite factorii declansatori sa-si poata evalua corect starea clinica (utilizind si peakflowmetrul) sa recunoasca semnele de agravare a bolii sa ceara ajutor medical corect LA NEVOIE sa nu intre in panica