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KEGAWAT DARURATAN SISTEM PERNAPASAN (SERANGAN ASMA AKUT, PNEUMONIA DAN COPD) dan EDEMA PARU
ASTHMA
Bronchus
Secretions
Wall thickening inflammation repair -- remodeling Loss of alveolar attachments Wall thinning inflammation elastolysis Coalescence Elasticity
ASTHMA
Bronchiole
Alveoli
TREATING ASTHMA
with Bronchodilators alone
is like
!!!
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Terkontrol
Maintain
Terkontrol
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
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Hospitalization or an ED visit for asthma in the past month Use of >2 canisters per month of inhaled short-acting beta2-agonist
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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 Inflammation and consolidation of lung tissue due to an infectious agent
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Outpatiet
Typical
Atypical
Inpatient
ICU
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PNEUMONIA/CAP
Merupakan infeksi saluran pernafasan 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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Inflammation & infection of lung- infecting organisms typically inhaled- organisms transmitted to lower airways and alveoli causing inflammation- impairs gas exchange Etiology: bacteria, virus, Mycoplasma, fungus, or from aspiration or inhalation of chemicals or other toxic substances Risk factors: cigarette smoking, chronic underlying disorders, severe acute illness, suppressed immune system, & immobility
Pneumonia pathogenesis
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PORT INDEX PNEUMONIA SEVERITY INDEX FOR COMMUNITY-ACQUIRED PNEUMONIA(CAP) Risk factor Demographics Men Women Nursing home resident Comorbidities Neoplasm Liver disease Heart failure Stroke Renal failure Physical examination findings Altered mental status Respiratory rate 30 breaths per minute Systolic blood pressure < 90 mm Hg Temperature < 95F (35C) or 104F (40C) Pulse rate 125 beats per minute Laboratory and radiographic findings Arterial pH < 7.35 Blood urea nitrogen > 30 mg per dL Sodium < 130 mmol per L Glucose 250 mg per dL Hematocrit < 30 percent Partial pressure of arterial oxygen < 60 mm Hg Pleural effusion Points Age (years): Age (years) - 10: +10
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Total Score
None 70 71-90 91-130 >130
Risk Class
I II III IV V
Treatment of CAP
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HAP
(Hospital Acquired Pneumonia/Nosocomial Pneumonia)/
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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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Usually progressive & irreversible; Ciliary cleansing mechanism of the respiratory tract is affected Involves 3 diseases- Chronic Bronchitis,
Risk factors- cigarette smoking, air pollution, occupational exposure, infections, allergens, stress 28
trachea
Emphysema bronchi
Chronic Bronchitis
alveoli
Asthma Response
Panel A
COPD Response
Panel B
COPD - SIGNS
HYPERINFLATION DECREASED EXPANSION CHEST PROLONGED EXPIRATION/WHEEZE SIGNS PULMONARY HYPERTENSION
Tripod position suggests distress, resting weight on knees helps with chest expansion
MANAGING EXACERBATIONS(Emergency)
ANTIBIOTICS CONTROLLED OXYGEN BRONCHODILATOR - BETA AGONIST
ANTICHOLINERGIC, THEOPHYLLINE STEROIDS INTUBATION/VENTILATION TREAT HEART FAILURE IF PRESENT (RESPIRATORY STIMULANTS?)
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INHALED ANTICHOLINERGICS, ANTIBIOTICS IPRATROPIUM BROMIDE OXITROPIUM BROMIDE TIOTROPIUM BROMIDE
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BETA 2 AGONIST COMBINATION INHALER
IPRATOPRIUM BROMIDE & SHORT ACTING INHALED BETA 2 AGONIST
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THEOPHYLLINE
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).
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.
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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tight junctions
Increased-permeability pulmonary edema, acute lung injury or acute respiratory distress syndrome
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Two Types
Cardiogenic (high pressure) Non-Cardiogenic (high permeability)
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Pulmonary Edema
High Pressure (cardiogenic)
AMI Chronic HTN Myocarditis
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EVALUATION
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History
Interstitial edema dyspnea and tachypnea Alveolar flooding hypoxemia, cough & expectoration of frothy edema fluid Unfortunately, the history is not always Focus on determining the underlying clinical disorder CARDIOGENIC: paroxysmal nocturnal dyspnea or orthopnea Ischemia myocardial infarction Exacerbation of chronic systolic or diastolic heart failure Dysfunction of the mitral or aortic valve Volume overload should also be considered NONCARDIOGENIC: signs & symptoms of infection, decrease in level of consciousness associated with vomiting, trauma etc. Pneumonia, Sepsis, Aspiration of gastric contents, Major trauma
reliable.
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THE END 57