*KEGAWAT DARURATAN SISTEM PERNAPASAN (SERANGAN ASMA AKUT, PNEUMONIA DAN COPD)

ASTHMA BRONCHIALE*

Asma- penyakit inflamasi kronikAsmaNormal

Wall thickening inflammation -- mucus gland hypertrophy Secretions Wall thinning - inflammation - elastolysisCoalescence ElasticityWall thickening inflammation repair -- remodelingLoss of alveolar attachments

*AntigenBarnes PJComplementary actions of long-acting b2-agonist(LABA) and corticosteroids on the pathophysiology of asthma.Reduction in Asthma AttackImprovement in the controlof Asthma symptoms

*Management of Asthma Exacerbations(Emergency)Inhaled beta2-agonist to provide prompt relief of airflow obstructionSystemic corticosteroids to suppress and reverse airway inflammationFor moderate-to-severe exacerbations, orFor patients who fail to respond promptly and completely to an inhaled beta2-agonist

Risk Factors for Death From AsthmaPast history of sudden severe exacerbationsPrior intubation or admission to ICU for asthmaTwo or more hospitalizations for asthma in the past yearThree or more ED visits for asthma in the past year*

Risk Factors for Death From Asthma (continued)Hospitalization or an ED visit for asthma in the past monthUse of >2 canisters per month of inhaled short-acting beta2-agonistCurrent use of systemic corticosteroids or recent withdrawal from systemic corticosteroids

Emergency Department and Hospital Management: Treatment After Repeat Assessment

FEV1 or PEF 50% to 80% predicted or personal best Physical exam: moderate symptomsInhaled short-acting beta2-agonist every 60 minutesSystemic corticosteroidContinue treatment 1 to 3 hours, provided there is improvement

Emergency Department and Hospital Management: Treatment After Repeat Assessment (continued)

FEV1 or PEF

Emergency Department and Hospital Management:Good Response

FEV1 or PEF >70%Response sustained 60 minutes after last treatmentNo distressPhysical exam: normalDischarge HomeDistrss:bhya Sustd: trs mnerus

Emergency Department and Hospital Management:Incomplete ResponseFEV1 or PEF >50% but

Emergency Department and Hospital Management:Poor Response

FEV1 or PEF 42 mm HgPhysical exam: symptoms severe, drowsiness, confusionAdmit to hospital intensive care

*Admit to Hospital Intensive CareInhaled beta2-agonist hourly or continuously + inhaled anticholinergicIV corticosteroidOxygenPossible intubation and mechanical ventilationAdmit to hospital ward

*

Step Up and Step Down Therapy of AsthmaReliever:Rapid-acting inhaled 2-agonist prnController:Daily inhaledcorticosteroid Controller:Daily inhaled corticosteroid Daily long-acting inhaled 2-agonistController:Daily inhaled corticosteroid Daily long acting inhaled 2-agonistplus (if needed)

When asthma is controlled, reduce therapy

MonitorSTEP DownOutcome: Asthma ControlOutcome: Best Possible ResultsController:None -Theophylline-SR -Leukotriene -Long-acting inhaled 2- agonist -Oral corticosteroid

PNEUMONIADEFINITION

Inflammation and consolidation of lungtissue due to an infectious agent *

Outpatiet

Inpatient

ICU

*COMMUNITY ACQUIRED (CAP)HOSPITAL ACQUIRED(HAP) AtypicalTypical

*

PNEUMONIA/CAPMerupakan infeksi saluran nafas bagian bawah (ISPB)SEAMIC Health Statistic 2001 penyebab kematian nomer 6 di IndonesiaSKRT Depkes 2001 ISPB penyebab kematian nomer 2 di IndonesiaSeorang dokter umum(ugd) harus mampu mengenali dan mendiagnosis penyakit ini*

DefinitionPneumonia is infection of the gas exchanging (alveolar) compartment of the lung (that is, it is a lower respiratory tract infection)

(Bronchitis is infection of the bronchial tree)(Tracheitis or pharyngitis are infections of the trachea or pharynx respectively)*

Pneumonia pathogenesis*

Pneumonia in immunocompetent patientsCommunity-acquired pneumoniaHospital-acquired pneumonia (also called nosocomial pneumonia)

Pneumonia in immunocompromised patients*

*Treatment of CAP

HAP (Hospital Acquired Pneumonia/Nosocomial Pneumonia)/*

Diagnosa HAP/Hospital Acquired Pneumonia)(Emergency)ATS (American thoracic Society, 1996). Bila gejala pneumonia, terjadi 48-72 jam penderita masuk rumah sakit, disebut HAP (dan diperkuat)dengan:Infiltrat baru atau perubahan infiltrat selagi terjadi onset baruHipo/hipertermiProduksi sputumLekositosis/lekopenia (Staufler, 1996)Oleh karena yang dirawat di ICU tidak selalu ada gambaran diatas, dibuat penelitian klinis CPIS (clinical pulmonary infection score)/VAP*

MANAGEMENT

Antibiotic therapy is the cornerstone of treatment for both CAP and HAP.

Initial therapy should be instituted rapidly.

Patients should initially be treated empirically, based on the severity of disease and the likely pathogens.

*

Treatment of Early Onset HAP*

Treatment of Late Onset HAP*

Treatment of HAP: Group 1No risk factors for resistance+ mild-moderate presentation

Treatment: 3rd generation non-pseudomonal cephalosporin(eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV)or 4th generation cephalosporin (cefepime 1-2g q12h IV) ORbeta-lactam/beta-lactamase inhibitor(eg. piperacillin-tazobactam 4.5 g q8h IV) ORfluoroquinolone (levofloxacin 750 mg IV qd or moxifloxacin 400 mg IV qd) po *

Treatment of HAP: Group 2 Risk factors for resistance, and/or late onset + mild-moderate presentation (Contd)

Treatment:3rd generation non-pseudomonal cephalosporin (eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV) or 4th generation cephalosporin (cefepime 1-2 g q12h IV) ORpiperacillin-tazobactam 4.5 g q8h IVORimipenem 500 mg q6h IV ORmeropenem 500 mg q6h IVORlevofloxacin 750 mg q24h IV OR moxifloxacin 400 mg q24h IV +/- vancomycin 1 g q12h IV or linezolid 600 mg q12h IV *

HAP: Group 3-Severe Presentation (Hypotension, Need for Intubation, Sepsis Syndrome, Rapid Progression of Infiltrates or End Organ Dysfunction) and/or Risk for ResistanceTreatment: Treat with combination therapy: anti-pseudomonal cephalosporin (ceftazidime or cefepime 2 g q8h IV) or beta-lactam/beta-lactamase inhibitor (piperacillin-tazobactam 4.5 g q6h IV) or carbapenem (imipenem or meropenem 1g q8h IV or 1 g q8h IV) plus fluoroquinolone (ciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IV) or aminoglycoside (gentamicin or tobramycin 5-7mg/kg qd IV or amikacin 15-20 mg/kg qd IV) +/- vancomycin 1 g q12 h IV or linezolid 600 mg q12 h IV if MRSA present or suspected *

Treatment of VAP: Group 4No risk factors for resistance, early onset (

Treatment of VAP: Group 5Risk factors for resistance present +/- severe presentation

Treatment: ceftazidime 2 g q8h IV or cefepime 2g q8h IVOR imipenem-cilastatin 1 g q8h IV(ELASTYN)OR meropenem 1 g q8h IV OR piperacillin-tazobactam 4.5 g q6h IV PLUS ciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IVOR gentamicin or tobramycin 5-7 mg/kg q24h IV or amikacin 15-20 mg/kg q24h IV +/- vancomycin 1 g q12h IV or linezolid 600 mg q12h IV*

Chronic Obstructive Pulmonary Disease (COPD)A group of chronic, obstructive airflow diseases of the lungs. Also known as chronic airflow limitation (CAL)Usually progressive & irreversible; Ciliary cleansing mechanism of the respiratory tract is affectedInvolves 3 diseases- Chronic Bronchitis, Asthma, & Emphysema

Risk factors- cigarette smoking, air pollution, occupational exposure, infections, allergens, stress

A group of chronic, obstructive airflow diseases of the lungs. Also known as chronic airflow limitation (CAL)Usually progressive & irreversible; Ciliary cleansing mechanism of the respiratory tract is affectedInvolves 3 diseases- Chronic Bronchitis, Asthma, & Emphysema

Risk factors- cigarette smoking, air pollution, occupational exposure, infections, allergens, stress

*

COPD

Expanded View of Etiology, Pathogenesis and Pathology in COPD

Cigarette smokeAlveolar macrophageNeutrophil PROTEASES Alveolar wall destruction(Emphysema)Mucus hypersecretion(Chronic bronchitis)PROTEASEINHIBITORSNeutrophil chemotactic factors CELLULAR MECHANISMS OF COPD Neutrophil elastaseCathepsinsMatrix metalloproteinasesCytokines (IL-8)Mediators (LTB4)4))?CD8+lymphocyte-MCP-1*

COPD - SIGNSHYPERINFLATIONDECREASED EXPANSION CHESTPROLONGED EXPIRATION/WHEEZESIGNS PULMONARY HYPERTENSION AND/OR RVH ( CARDIAC FAILURE)CYANOSISHYPERCAPNIA - ASTERIXUS, (PRE)-COMA*

Expanded View of Etiology, Pathogenesis and Pathology in COPD

MANAGING EXACERBATIONSANTIBIOTICSCONTROLLED OXYGENBRONCHODILATOR - BETA AGONIST ANTICHOLINERGIC, THEOPHYLLINESTEROIDSNIV BIPAPINTUBATION/VENTILATIONTREAT HEART FAILURE IF PRESENT(RESPIRATORY STIMULANTS?)

BRONCHODILATORSFOR COPDIPRATROPIUM BROMIDEOXITROPIUM BROMIDETIOTROPIUM BROMIDEINHALEDANTICHOLINERGICSIPRATOPRIUM BROMIDE&SHORT ACTING INHALEDBETA 2 AGONISTSHORT ACTING INHALED BETA 2 AGONISTBETA 2AGONISTCOMBINATIONINHALER123THEOPHYLLINE4

Antibiotics

Acute exacerbations of COPD are commonly assumed to be due to bacterial infection, since they may be associated with increased volume and purulence of the sputum.Exacerbations may be due to viral infections of the upper respiratory tract or may be noninfective, so that antibiotic treatment is not always warranted.

*

AntibioticsA meta-analysis of controlled trials of antibiotics in COPD showed a statistically significant but small benefit of antibiotics in terms of clinical outcome and lung function. Although antibiotics are still widely used for exacerbations of COPD, methods to diagnose bacterial infection reliably in the respiratory tract are needed so that antibiotics are not used inappropriately. There is no evidence that prophylactic antibiotics prevent acute exacerbations*

Oxygen

Long-term oxygen therapy:reduced mortality improvement in quality of life in patients with severe COPD and chronic hypoxemia (partial pressure of arterial oxygen,

CorticosteroidsInhaled corticosteroids are now the mainstay of therapy for chronic asthma, However, the inflammation in COPD is not suppressed by inhaled or oral corticosteroids, even at high doses. This lack of effect may be due to the fact that corticosteroids prolong the survival of neutrophils and do not suppress neutrophilic inflammation in COPD. *

Approximately 10 percent of patients with stable COPD have some symptomatic and objective improvement with oral corticosteroids. It is likely that these patients have concomitant asthma, since both diseases are very common. Indeed, airway hyperresponsiveness, a characteristic of asthma, may predict an accelerated decline in FEV1 in patients with COPD. *

long-term treatment with high doses of inhaled corticosteroids reduced the progression of COPD, even when treatment was started before the disease became symptomatic. Inhaled corticosteroids may slightly reduce the severity of acute exacerbations, but it is unlikely that their use can be justified in view of the risk of systemic side effects in these susceptible patients and the expense of using high-dose inhaled corticosteroids for several years. *

Manage ExacerbationsKey PointsExacerbations of respiratory symptoms requiring medical intervention are important clinical events in COPD.

The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B).

Manage ExacerbationsKey PointsInhaled bronchodilators (beta2-agonists and/or anticholinergics), theophylline, and systemic, preferably oral, glucocortico-steroids are effective for the treatment of COPD exacerbations (Evidence A).

Manage ExacerbationsKey PointsPatients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased volume and change of color of sputum, and/or fever) may benefit from antibiotic treatment (Evidence B).

*Thanks for your attention!!

Prof Baramwioct 2009*oct 2009Prof Baramwioct 2009*Slide 13Asthma is a chronic inflammatory disorder of the airwaysThis bronchoscopic view of an airway shows the normal appearance of a healthy airway,contrasted with inflammation (reddening and swelling) and narrowing of the asthmatic airwayMicroscopic examination of biopsy and lavage samples taken through the bronchoscope hasestablished that inflammatory changes are present in asthma of all grades of severity,including recently diagnosed asthmaoct 2009Prof Baramwioct 2009*Clear understanding of the structure and function of the organ involved makes it easy to explain COPD symptomatologyThe large airways: The larger branches with cartilagenous support are called bronchi and the smaller tubes without cartilage are called bronchioles.The first 16-17 generation branches serve only to conduct the air (the conducting zone). There is no gas diffusion into or out of the body in the airways. Its cartilagenous wall prevents the inflammation from spilling out into the lung parenchymaThe airways maintain their patency from their structure:Reid Index: the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and cartilage (N.V. = < 0.4 )The peripheral airways become the major site of airways obstruction in COPD. The structural changes in the airway wall are the most importantcause of the increase in peripheral airways resistance in COPD. Inflammatory changes such as airway edema and mucus hypersecretion alsocontribute to airway narrowing. The small airways:The definition of small airways is all airways less than 2 mm in diameter. They're airways without cartilage and glands. They include the parenchyma and alveolar tissue, and they're poorly understood physiologically and pathophysiologically. Saetta et al. ERJ 1994: Small airways in smokers:- epithelial abnormalities- inflammed walls- increased muscle- increased fibrosis- less alveolar attachments- hyper responsive to non-specific stimuliAlveoli:Alveolar wall destruction (elastolysis) instead of thickening! Macrophages and neutrophils accumulate and release elastins and matrix metalloproteinase-9 (MMP-9) leading to loss of lung elasticity.There is a chronic inflammation that leads to fixed narrowing of small airways andalveolar wall destruction (emphysema). This is characterised by increased numbers ofalveolar macrophages, neutrophils and cytotoxic T-lymphocytes, and the release ofmultiple inflammatory mediators (lipids, chemokines, cytokines, growth factors). Ahigh level of oxidative stress may amplify this inflammation. There is also increasedelastolysis and evidence for involvement of several elastolytic enzymes, including serineproteases, cathepsins and matrix metalloproteinases. Chronic obstructive pulmonary disease: molecular and cellular mechanisms.P.J. Barnes, S.D. Shapiro, R.A. Pauwels. #ERS Journals Ltd 2003

Most common in COPD patients is the centrilobular form of emphysema, which involves dilatation and destruction of the respiratory bronchioles. Physiological changes characteristic of the disease include mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation,gas exchange abnormalities, pulmonary hypertension, and cor pulmonale, and they usually develop in this order over the course of the disease. The irreversible component of airflow limitation is primarily due to remodeling of the small airways. Parenchymal destruction (emphysema) also contributes but plays a smaller role.

oct 2009Prof Baramwioct 2009* Most patients with asthma require two major therapies: an inhaled 2-agonist and an inhaled corticosteroid 2-agonists act mainly by relaxing the airway smooth muscle, but because they also stabilise mast cells they may block the early reaction to triggers, such as allergens and exercise Corticosteroids are highly effective at suppressing the various components of inflammation, with effects on macrophages, eosinophils and T-lymphocytes. These effects lead to a reduction in airway hyperresponsiveness and a resultant improvement in the control of asthma symptomsoct 2009Prof Baramwioct 2009*3oct 2009Prof Baramwioct 2009*5oct 2009Prof Baramwioct 2009*6oct 2009Prof Baramwioct 2009*32oct 2009Prof Baramwioct 2009*33oct 2009Prof Baramwioct 2009*34oct 2009Prof Baramwioct 2009*35oct 2009Prof Baramwioct 2009*36oct 2009Prof Baramwioct 2009*37oct 2009Prof Baramwioct 2009*oct 2009Prof Baramwioct 2009*oct 2009*Expanded view of etiology:- smoking the most important cause of COPD but it is not the only one: in rural communities, use of biomass fuel for cooking has been identified as a cause of COPD (equivalent to 2 packs/day smoking!)- focusing as well to these other causes does not remove our attention to the smoking problem- consideration to non-smoking COPD is a service the we should provide it may help get COPD the attention it deservesCOPD pathogenesis:- a pattern is emerging: noxious stimulation chronic inflammation Destruction, repair and remodeling abnormal function symptoms- this is modulated by: genetics, load of exposure- the manifestation related to the structure that is affected: large airway, small airway, alveoli. Also, COPD is a systemic disease, hence, with non-pulmonary symptoms (weight loss, muscle function impairment, ect)oct 2009*Expanded view of etiology:- smoking the most important cause of COPD but it is not the only one: in rural communities, use of biomass fuel for cooking has been identified as a cause of COPD (equivalent to 2 packs/day smoking!)- focusing as well to these other causes does not remove our attention to the smoking problem- consideration to non-smoking COPD is a service the we should provide it may help get COPD the attention it deservesCOPD pathogenesis:- a pattern is emerging: noxious stimulation chronic inflammation Destruction, repair and remodeling abnormal function symptoms- this is modulated by: genetics, load of exposure- the manifestation related to the structure that is affected: large airway, small airway, alveoli. Also, COPD is a systemic disease, hence, with non-pulmonary symptoms (weight loss, muscle function impairment, ect)oct 2009