Professional Documents
Culture Documents
Bronchus
Secretions
Wall thickening inflammation repair -- remodeling
Bronchiole
Alveoli
2-Agonists
BRONCHOCONSTRICTION
Airway smooth muscle Eosinophil
Antigen
Macrophage
Corticosteroids
Complementary actions of long-acting b2-agonist(LABA) and corticosteroids on the pathophysiology of asthma.
For moderate-to-severe exacerbations, or For patients who fail to respond promptly and completely to an inhaled beta2-agonist
6
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
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
14
Controller:
Controller: Controller:
None
Controller:
Daily inhaled corticosteroid
Daily inhaled corticosteroid Daily long acting inhaled 2-agonist plus (if needed)
STEP Down
15
PNEUMONIA
DEFINITION Inflammation and consolidation of lung tissue due to an infectious agent
16
Outpatiet
Typical
Atypical
Inpatient
ICU
17
18
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
19
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
20
Pneumonia pathogenesis
21
nosocomial pneumonia)
22
Treatment of CAP
23
24
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.
26
27
28
29
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
31
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
35
COPD
Cigarette smoke
CD8+ lymphocyte
Alveolar macrophage
MCP-1
COPD - SIGNS
HYPERINFLATION DECREASED EXPANSION CHEST PROLONGED EXPIRATION/WHEEZE SIGNS PULMONARY HYPERTENSION
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
2
BETA 2 AGONIST COMBINATION INHALER
IPRATOPRIUM BROMIDE & 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.
43
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
44
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
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
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.
48
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).