kegawatan asthma ,pneumonia copd
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ASTHMA
BRONCHIALE
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Asma- penyakit inflamasi kronik
AsmaNormal
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Bronchus
Wall thickening
inflammation -
- mucus gland
hypertrophy
Secretions
Alveoli
Wall thinning -
inflammation -
elastolysis
Coalescence
Elasticity
Bronchiole
Wall thickening
inflammation
repair-- remodeling
Loss of alveolar
attachments
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Antigen
2-Agonists
Corticosteroids
Virus?
Virus?
Adenosine
ExerciseFog
AIRWAY
HYPERRESPONSIVENESS
BRONCHOCONSTRICTION
Mast cel l A i rway smooth mu sc le
Macrophage Eos inoph i l
- lymphocyte
Barnes PJ
Complementary actions of long-acting b2-agonist(LABA) and
corticosteroids on the pathophysiology of asthma.
Reduction in Asthma Attack
Improvement in the control
of Asthma symptoms
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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
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Risk Factors for
Death From Asthma(continued)
Hospitalization or an ED visit for asthma
in the past month
Use of >2 canistersper month of inhaled
short-acting beta2-agonist
Current use of systemic corticosteroidsor recent withdrawal from systemic
corticosteroids
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Emergency Department and Hospital
Management: Treatment After Repeat
Assessment
FEV1or PEF 50% to 80% predicted
or personal best
Physical exam: moderate
symptoms
Inhaled short-acting beta2-agonistevery 60 minutes
Systemic corticosteroid
Continue treatment 1 to 3 hours,
provided there is improvement
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Emergency Department and Hospital
Management: Treatment After Repeat
Assessment (continued) FEV1or PEF
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Emergency Department and Hospital
Management:
Good Response
FEV1or PEF >70%
Response sustained 60 minutes
after last treatment No distress
Physical exam: normal
Discharge Home
Distrss:bhya Sustd: trs mnerus
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Emergency Department and Hospital
Management:
Incomplete Response
FEV1
or PEF >50% but
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Emergency Department and Hospital
Management:
Poor Response
FEV1or PEF 42 mm Hg
Physical exam: symptoms severe,drowsiness, confusion
Admit to hospital intensive care
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dmit to Hospital IntensiveCare 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 Upand Step Down Therapy ofAsthma
Reliever: Rapid-acting inhaled 2-agonist prn
Controller:
Daily inhaled
corticosteroid
Controller:
Daily inhaledcorticosteroid
Daily long-acting inhaled2-agonist
Controller:
Daily inhaled
corticosteroid Daily long
acting inhaled2-agonist
plus (if needed)
Whenasthma iscontrolled,reducetherapy
Monitor
STEP Down
Outcome: Asthma Control Outcome: BestPossible Results
Controller:
None-Theophylline-SR
-Leukotriene
-Long-acting inhaled
2- agonist-Oral corticosteroid
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PNEUMONIA
DEFINITION
Inflammation and consolidation of lung
tissue due to an infectious agent
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Outpatiet
Inpatient
ICU
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COMMUNITYACQUIRED (CAP)
HOSPITAL ACQUIRED
(HAP)
AtypicalTypical
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PNEUMONIA/CAP
Merupakan infeksi saluran nafas bagianbawah (ISPB)
SEAMIC Health Statistic 2001
penyebab kematian nomer 6di Indonesia SKRT Depkes 2001ISPB penyebab
kematian nomer 2di Indonesia
Seorang dokter umum ugd) harusmampu mengenali danmendiagnosis penyakit ini
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Definition
Pneumonia is infection of the gas exchanging(alveolar) compartment of the lung (that is, itis 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
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Pneumonia in immunocompetent patients
Community-acquired pneumonia
Hospital-acquired pneumonia (also callednosocomial pneumonia)
Pneumonia inimmunocompromised patients
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T t t f CAP
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Treatment of CAP
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HAP(Hospital Acquired
Pneumonia/Nosocomial
Pneumonia)/
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Diagnosa HAP/Hospital Acquired
Pneumonia)(Emergency) ATS (American thoracic Society, 1996). Bila gejala
pneumonia, terjadi 48-72 jam penderita masuk rumahsakit, disebut HAP (dan diperkuat)dengan:
Infiltrat baru atau perubahan infiltrat selagi terjadi onsetbaru
Hipo/hipertermi
Produksi sputum
Lekositosis/lekopenia (Staufler, 1996)
Oleh karena yang dirawat di ICU tidak selalu adagambaran diatas, dibuat penelitian klinis CPIS (clinicalpulmonary infection score)/VAP
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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, basedon the severity of disease and the likely pathogens.
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T t t f E l O t HAP
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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-moderatepresentation
Treatment:
3rdgeneration non-pseudomonal cephalosporin(eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV)
or 4thgeneration 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 29
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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 4thgeneration cephalosporin (cefepime 1-2 g q12h IV)
ORpiperacillin-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 IV30
HAP: Group 3-Severe Presentation (Hypotension, Need
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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 orcefepime 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 gq8h IV)
plusfluoroquinolone (ciprofloxacin 400 mg q8h IV or
levofloxacin 750 mg q24h IV)or
aminoglycoside (gentamicin or tobramycin 5-7mg/kg qdIV or amikacin 15-20 mg/kg qd IV)
+/-
vancomycin 1 g q12 h IV or linezolid 600 mg q12 h IV ifMRSA present or suspected 31
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Treatment of VAP: Group 4
No risk factors for resistance, early onset (
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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
PLUSciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IV
OR
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
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Chronic Obstructive Pulmonary
Disease (COPD)
A group of chronic, obstructive airflow diseases of thelungs. Also known as chronic airflow limitation(CAL)
Usually progressive & irreversible; Ciliary cleansingmechanism of the respiratory tract is affected
Involves 3 diseases- Chronic Bronchitis, Asthma, &Emphysema
Risk factors- cigarette smoking, air pollution,occupational exposure, infections, allergens, stress
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A group of chronic, obstructiveairflow diseases of the lungs. Alsoknown as chronic airflow limitation(CAL)
Usually progressive & irreversible;Ciliary cleansing mechanism of therespiratory tract is affected
Involves 3 diseases- Chronic
Bronchitis, Asthma, & Emphysema
Risk factors- cigarette smoking, airpollution, occupational exposure,infections, allergens, stress 35
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COPD
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Expanded View of Etiology, Pathogenesis
and Pathology in COPD
Noxiousstimulation
Chronic
inflammation
Destruction,
repair andremodeling
Abnormal function
and symptoms
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Cigarette smoke
Alveolar m acrophage
Neutrophi l
PROTEASES
Alveolar wall destruction
(Emphysema)
Mucus hypersecretion
(Chronic bronchitis)
PROTEASEINHIBITORS
Neutrophil chemotactic factors
CELLULAR MECHANISMS OF COPD
Neutrophil elastaseCathepsins
Matrix metalloproteinases
Cytokines (IL-8)Mediators (LTB4)4))
?CD8+
lymphocy te
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MCP-1
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COPD - SIGNS
HYPERINFLATION
DECREASED EXPANSION CHEST
PROLONGED EXPIRATION/WHEEZESIGNS PULMONARY HYPERTENSION
AND/OR RVH ( CARDIAC FAILURE)
CYANOSIS
HYPERCAPNIA - ASTERIXUS, (PRE)-COMA
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E d d Vi f E i l P h i d
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Expanded View of Etiology, Pathogenesis and
Pathology in COPD
Noxious stimulation
Chronic
inflammation
Destruction,
repair and
remodeling
Abnormal function
and symptoms
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MANAGING
EXACERBATIONS
ANTIBIOTICS
CONTROLLED OXYGEN
BRONCHODILATOR - BETA AGONIST
ANTICHOLINERGIC, THEOPHYLLINE STEROIDS
NIV BIPAP
INTUBATION/VENTILATION
TREAT HEART FAILURE IF PRESENT
(RESPIRATORY STIMULANTS?)
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BRONCHODILATORS
FOR COPD
IPRATROPIUM BROMIDEOXITROPIUM BROMIDETIOTROPIUM BROMIDE
INHALEDANTICHOLINERGIC
S
IPRATOPRIUM BROMIDE&
SHORT ACTING INHALEDBETA 2 AGONIST
SHORT ACTING INHALEDBETA 2 AGONIST
BETA 2AGONIST
COMBINATIONINHALER
1
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THEOPHYLLINE
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Antibiotics
Acute exacerbations of COPD are commonlyassumed to be due to bacterial infection, sincethey may be associated with increased volumeand purulence of the sputum.
Exacerbations may be due to viral infections ofthe upper respiratory tract or may benoninfective, so that antibiotic treatment is not
always warranted.
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Antibiotics
A meta-analysis of controlled trials of antibioticsin COPD showed a statistically significant butsmall benefit of antibiotics in terms of clinicaloutcome and lung function.
Although antibiotics are still widely used forexacerbations of COPD, methods to diagnosebacterial infection reliably in the respiratory tractare needed so that antibiotics are not used
inappropriately. There is no evidence thatprophylactic antibiotics prevent acuteexacerbations
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Oxygen
Long-term oxygen therapy:
reduced mortality
improvement in quality of life in patientswith severe COPD and chronic hypoxemia(partial pressure of arterial oxygen,
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Corticosteroids
Inhaled corticosteroids are now the mainstay oftherapy for chronic asthma,
However, the inflammation in COPD is not
suppressed by inhaled or oral corticosteroids, even athigh doses.
This lack of effect may be due to the fact that
corticosteroids prolong the survival of neutrophils
and do not suppress neutrophilic inflammation inCOPD.
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Approximately 10 percent of patients withstable COPD have some symptomatic and
objective improvement with oralcorticosteroids. It is likely that thesepatients have concomitant asthma, sinceboth diseases are very common. Indeed,
airway hyperresponsiveness, acharacteristic of asthma, may predict anaccelerated decline in FEV1in patients withCOPD.
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long-term treatment with high doses of inhaled
corticosteroids reduced the progression of COPD,even when treatment was started before thedisease became symptomatic.
Inhaled corticosteroids may slightly reduce the
severity of acute exacerbations, but it is unlikelythat their use can be justified in view of the risk ofsystemic side effects in these susceptible patientsand the expense of using high-dose inhaled
corticosteroids for several years.
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Manage Exacerbations
Key Points
Exacerbations of respiratory symptomsrequiring medical intervention are importantclinical events in COPD.
The most common causes of an exacerbationare infection of the tracheobronchial tree and
air pollution, but the cause of about one-third of severe exacerbations cannot beidentified(Evidence B).
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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).
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Manage Exacerbations
Key Points
Patients experiencing COPD
exacerbations with clinical signs of
airway infection (e.g., increased volumeand change of color of sputum, and/or
fever) may benefit from antibiotic
treatment(Evidence B).
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Thanks for your attention!!