ASTHMA BRONCHIALE

Asma- penyakit inflamasi kronik

Normal Asma

Wall thickening inflammation - mucus gland hypertrophy

Bronchus

Secretions
Wall thickening inflammation repair -- remodeling

Bronchiole

Loss of alveolar attachments Wall thinning inflammation elastolysis Coalescence Elasticity

Alveoli

Virus? Adenosine Exercise Fog

Mast cell

2-Agonists

BRONCHOCONSTRICTION
Airway smooth muscle Eosinophil

Antigen
Macrophage

AIRWAY HYPERRESPONSIVENESS Virus?

-lymphocyte

Reduction in Asthma Attack Improvement in the control of Asthma symptoms

Barnes PJ

Corticosteroids
Complementary actions of long-acting b2-agonist(LABA) and corticosteroids on the pathophysiology of asthma.

Management of Asthma Exacerbations(Emergency)

Inhaled beta2-agonist to provide prompt relief of airflow obstruction

Systemic corticosteroids to suppress and reverse airway inflammation

For moderate-to-severe exacerbations, or For patients who fail to respond promptly and completely to an inhaled beta2-agonist
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Risk Factors for Death From Asthma

Past history of sudden severe exacerbations Prior intubation or admission to ICU for asthma Two or more hospitalizations for asthma in the past year Three 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 month Use of >2 canisters per month of inhaled short-acting beta2-agonist

Current 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 symptoms Inhaled short-acting beta2-agonist every 60 minutes Systemic corticosteroid Continue treatment 1 to 3 hours, provided there is improvement

Emergency Department and Hospital Management: Treatment After Repeat Assessment (continued)
FEV1 or PEF <50% predicted or personal best Physical exam: severe symptoms at rest, accessory muscle use, chest retraction History: high-risk patient No improvement after initial treatment

Oxygen Inhaled short-acting beta2-agonist hourly or continuously + inhaled anticholinergic Systemic corticosteroid

Emergency Department and Hospital Management: Good Response

FEV1 or PEF >70% Response sustained 60 minutes after last treatment No distress Physical exam: normal Discharge Home

Distrss:bhya Sustd: trs mnerus

Emergency Department and Hospital Management: Incomplete Response

FEV1 or PEF >50% but <70% Mild-to-moderate symptoms

Individualized decision re: hospitalization

Emergency Department and Hospital Management: Poor Response

FEV1 or PEF <50% PCO2 >42 mm Hg Physical exam: symptoms severe, drowsiness, confusion

Admit to hospital intensive care

Admit to Hospital Intensive Care

Inhaled beta2-agonist hourly or continuously + inhaled anticholinergic IV corticosteroid Oxygen Possible intubation and mechanical ventilation

Admit to hospital ward

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Step Up and Step Down Therapy of Asthma

Outcome: Asthma Control
Outcome: Best Possible Results

Controller:

Controller: Controller:
None

Controller:
Daily inhaled corticosteroid

Daily inhaled corticosteroid Daily longacting inhaled 2-agonist

Daily inhaled corticosteroid Daily long acting inhaled 2-agonist plus (if needed)

When asthma is controlled, reduce therapy Monitor

-Theophylline-SR -Leukotriene -Long-acting inhaled 2- agonist -Oral corticosteroid

Reliever: Rapid-acting inhaled 2-agonist prn

STEP Down

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PNEUMONIA
DEFINITION Inflammation and consolidation of lung tissue due to an infectious agent

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COMMUNITY ACQUIRED (CAP)

Outpatiet

Typical

Atypical

Inpatient

HOSPITAL ACQUIRED (HAP)

ICU
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PNEUMONIA/CAP
Merupakan infeksi saluran nafas bagian bawah (ISPB) SEAMIC Health Statistic 2001 penyebab kematian nomer 6 di Indonesia SKRT Depkes 2001 ISPB penyebab kematian nomer 2 di Indonesia

Seorang dokter umum(ugd) harus

mampu mengenali dan mendiagnosis penyakit ini

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Definition
Pneumonia 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)

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Pneumonia pathogenesis

21

Pneumonia in immunocompetent patients

Community-acquired pneumonia Hospital-acquired pneumonia (also called

nosocomial pneumonia)

Pneumonia in immunocompromised patients

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Treatment of CAP

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HAP (Hospital Acquired

Pneumonia/Nosocomial Pneumonia)/

24

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 baru Hipo/hipertermi Produksi sputum Lekositosis/lekopenia (Staufler, 1996) Oleh karena yang dirawat di ICU tidak selalu ada gambaran diatas, dibuat penelitian klinis CPIS (clinical pulmonary infection score)/VAP

25

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.

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Treatment of Early Onset HAP

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Treatment of Late Onset HAP

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Treatment of HAP: Group 1

No 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) OR beta-lactam/beta-lactamase inhibitor (eg. piperacillin-tazobactam 4.5 g q8h IV) OR fluoroquinolone (levofloxacin 750 mg IV qd or moxifloxacin 400 mg IV qd) po

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Treatment of HAP: Group 2

Risk factors for resistance, and/or late onset + mildmoderate 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) OR piperacillin-tazobactam 4.5 g q8h IV OR imipenem 500 mg q6h IV OR meropenem 500 mg q6h IV OR levofloxacin 750 mg q24h IV OR moxifloxacin 400 mg q24h IV +/vancomycin 1 g q12h IV or linezolid 600 mg q12h IV 30

Treatment: Treat with combination therapy: anti-pseudomonal cephalosporin (ceftazidime or cefepime 2 g q8h IV) or beta-lactam/beta-lactamase inhibitor (piperacillintazobactam 4.5 g q6h IV) or carbapenem (imipenem or meropenem 1g q8h IV or 1 g q8h IV) 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

HAP: Group 3-Severe Presentation (Hypotension, Need for Intubation, Sepsis Syndrome, Rapid Progression of Infiltrates or End Organ Dysfunction) and/or Risk for Resistance

plus

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Treatment of VAP: Group 4

No risk factors for resistance, early onset (<5 days of hospitalization) & moderate presentation Treatment: 3rd generation non-pseudomonal cephalosporin (eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV) or 4th generation cephalosporin (cefepime 2 g q12h IV) OR beta-lactam/beta-lactamase inhibitor (eg. piperacillin-tazobactam 4.5 g q6h IV) OR fluoroquinolone (levofloxacin 750 mg IV qd, moxifloxacin 400 mg IV qd] po
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Treatment of VAP: Group 5

Risk factors for resistance present +/- severe presentation Treatment: ceftazidime 2 g q8h IV or cefepime 2g q8h IV OR imipenem-cilastatin 1 g q8h IV(ELASTYN) OR meropenem 1 g q8h IV OR piperacillin-tazobactam 4.5 g q6h IV ciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IV OR gentamicin or tobramycin 5-7 mg/kg q24h IV or amikacin 1520 mg/kg q24h IV +/vancomycin 1 g q12h IV or linezolid 600 mg q12h IV
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PLUS

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 affected Involves 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

Usually progressive & irreversible; Ciliary cleansing mechanism of the respiratory tract is affected Involves 3 diseases- Chronic

known as chronic airflow limitation (CAL)

Bronchitis, Asthma, & Emphysema

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

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COPD

Expanded View of Etiology, Pathogenesis and Pathology in COPD

Noxious stimulation Chronic inflammation Destruction, repair and remodeling Abnormal function and symptoms

CELLULAR MECHANISMS OF COPD

Cigarette smoke

CD8+ lymphocyte

Alveolar macrophage
MCP-1

Neutrophil chemotactic factors Cytokines (IL-8) Mediators (LTB4) 4))

Neutrophil PROTEASE INHIBITORS

Neutrophil elastase Cathepsins PROTEASES Matrix metalloproteinases

Alveolar wall destruction (Emphysema)

Mucus hypersecretion (Chronic bronchitis) 38

COPD - SIGNS
HYPERINFLATION DECREASED EXPANSION CHEST PROLONGED EXPIRATION/WHEEZE SIGNS PULMONARY HYPERTENSION

AND/OR RVH ( CARDIAC FAILURE) CYANOSIS HYPERCAPNIA - ASTERIXUS, (PRE)COMA

39

Expanded View of Etiology, Pathogenesis and Pathology in COPD

Noxious stimulation Chronic inflammation Destruction, repair and remodeling Abnormal function and symptoms

MANAGING EXACERBATIONS
ANTIBIOTICS CONTROLLED OXYGEN BRONCHODILATOR - BETA AGONIST ANTICHOLINERGIC, THEOPHYLLINE STEROIDS NIV BIPAP INTUBATION/VENTILATION TREAT HEART FAILURE IF PRESENT (RESPIRATORY STIMULANTS?)

1 INHALED ANTICHOLINERGIC S
IPRATROPIUM BROMIDE OXITROPIUM BROMIDE TIOTROPIUM BROMIDE

BRONCHODILATORS FOR COPD

3

2
BETA 2 AGONIST COMBINATION INHALER
IPRATOPRIUM BROMIDE & SHORT ACTING INHALED BETA 2 AGONIST

SHORT ACTING INHALED BETA 2 AGONIST

4 THEOPHYLLIN E

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.

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Antibiotics
A 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
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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, <55 mm Hg).

45

Corticosteroids
Inhaled 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.

46

 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.

47

 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.

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Manage Exacerbations Key Points

Exacerbations 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 onethird of severe exacerbations cannot be identified (Evidence B).

Manage Exacerbations Key Points

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

Manage Exacerbations Key Points

Patients 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!!

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