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KEGAWAT DARURATAN SISTEM PERNAPASAN (SERANGAN ASMA AKUT, PNEUMONIA DAN COPD)
ASTHMA BRONCHIALE
Bronchus
Secretions
Wall thickening inflammation repair -- remodeling
Bronchiole
Alveoli
2-Agonists
BRONCHOCONSTRICTION
Airway smooth muscle
Eosinophil
Antigen
Macrophage
AIRWAY HYPERRESPONSIVENESS
Virus?
-lymphocyte
of Asthma symptoms
Barnes PJ
Corticosteroids
Complementary actions of long-acting b2-agonist(LABA) and corticosteroids on the pathophysiology of asthma.
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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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
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
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
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Controller:
Controller: Controller:
None
Controller:
Daily inhaled corticosteroid
Daily inhaled corticosteroid Daily long acting inhaled 2-agonist plus (if needed)
STEP Down
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PNEUMONIA
DEFINITION
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Outpatiet
Typical
Atypical
Inpatient
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
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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
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Pneumonia pathogenesis
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nosocomial pneumonia)
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Treatment of CAP
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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: 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: 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: 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
(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
Usually progressive & irreversible; Ciliary cleansing mechanism of the respiratory tract is affected Involves 3 diseases- Chronic
Risk factors- cigarette smoking, air pollution, occupational exposure, infections, allergens, stress
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COPD
Cigarette smoke
CD8+ lymphocyte
Alveolar macrophage
MCP-1
PROTEASES
COPD - SIGNS
HYPERINFLATION DECREASED EXPANSION CHEST PROLONGED EXPIRATION/WHEEZE SIGNS PULMONARY HYPERTENSION
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
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BETA 2 AGONIST COMBINATION INHALER
IPRATOPRIUM BROMIDE & SHORT ACTING INHALED BETA 2 AGONIST
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).
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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.
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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.
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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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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).