kuliah 2 kegawatan asthma ,pneumonia copd,edema paru
TRANSCRIPT
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KEGAWAT DARURATANSISTEM PERNAPASAN(SERANGAN ASMA AKUT, PNEUMONIA DAN COPD)dan EDEMA PARU
ASTHMA
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Asma- penyakit inflamasi kronikAsma- penyakit inflamasi kronik
AsmaNormal
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
ASTHMA
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TREATING ASTHMA
with Bronchodilators alone
is like
Painting over rust !!!
Terapi Asma Masa DepanTerapi Asma Masa Depan
IntermitenIntermiten
Asma
Persisten
Tidak terkontrol
MaintainLABACS
Tujuan penatalaksanaan
asma :TOTAL KONTROL
Boushey H. Is Asthma Control Achieveable ?, European Respiratory Journal , Dec 2004
Terkontrol
Tidak terkontrol Terkontrol
Tingkatkan dosis
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Management of Asthma Management of Asthma Exacerbations(Emergency)Exacerbations(Emergency)
Inhaled betaInhaled beta22-agonist to provide prompt -agonist to provide prompt
relief of airflow obstructionrelief of airflow obstruction
Systemic corticosteroids to suppress and Systemic corticosteroids to suppress and reverse airway inflammationreverse airway inflammation
– For moderate-to-severe exacerbations, orFor moderate-to-severe exacerbations, or
– For patients who fail to respond promptly and For patients who fail to respond promptly and completely to an inhaled betacompletely to an inhaled beta22-agonist -agonist
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Risk Factors for Risk Factors for Death From AsthmaDeath From Asthma
Past history of sudden severe Past history of sudden severe exacerbationsexacerbations
Prior intubation or admission to ICUPrior intubation or admission to ICUfor asthmafor asthma
Two or more hospitalizations for asthmaTwo or more hospitalizations for asthmain the past yearin the past year
Three or more ED visits for asthmaThree or more ED visits for asthmain the past yearin the past year
Risk Factors for Risk Factors for Death From Asthma Death From Asthma (continued)(continued)
Risk Factors for Risk Factors for Death From Asthma Death From Asthma (continued)(continued)
Hospitalization or an ED visit for Hospitalization or an ED visit for asthmaasthmain the past monthin the past month
Use of Use of >2 canisters>2 canisters per month of per month of inhaled short-acting betainhaled short-acting beta22-agonist-agonist
Current use of systemic Current use of systemic corticosteroidscorticosteroidsor recent withdrawal from systemic or recent withdrawal from systemic corticosteroidscorticosteroids
Hospitalization or an ED visit for Hospitalization or an ED visit for asthmaasthmain the past monthin the past month
Use of Use of >2 canisters>2 canisters per month of per month of inhaled short-acting betainhaled short-acting beta22-agonist-agonist
Current use of systemic Current use of systemic corticosteroidscorticosteroidsor recent withdrawal from systemic or recent withdrawal from systemic corticosteroidscorticosteroids
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Admit to Hospital Admit to Hospital Intensive CareIntensive Care
• Inhaled betaInhaled beta22-agonist hourly or -agonist hourly or
continuously + inhaled anticholinergiccontinuously + inhaled anticholinergic• IV corticosteroidIV corticosteroid• OxygenOxygen• Possible intubation and mechanical Possible intubation and mechanical
ventilationventilation
• Admit to hospital wardAdmit to hospital ward
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Step Up and Step Down Therapy of AsthmaStep Up and Step Down Therapy of Asthma
Reliever: Rapid-acting inhaled β2-agonist prn
Controller: Daily inhaledcorticosteroid
Controller: Daily inhaled
corticosteroid Daily long-
acting inhaled β2-agonist
Controller: Daily inhaled
corticosteroid Daily long –
acting inhaled β2-agonist
plus (if needed)
When asthma is controlled, reduce therapy
Monitor
STEP DownSTEP DownSTEP DownSTEP Down
Outcome: Asthma Control Outcome: Best Possible Results
Controller:None
-Theophylline-SR -Leukotriene -Long-acting inhaled β2- agonist -Oral corticosteroid
PNEUMONIAPNEUMONIA
DEFINITION
Inflammation and consolidation of lung
tissue due to an infectious agent
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Outpatiet
Inpatient
ICU
Outpatiet
Inpatient
ICU
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COMMUNITY ACQUIRED (CAP)
HOSPITAL ACQUIRED
(HAP)
AtypicalTypical
PNEUMONIA/CAPPNEUMONIA/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
• Seorang dokter umum(ugd) harus mampu mengenali dan mendiagnosis penyakit ini
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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
Bacterial pneumonia. Klebsiella pneumoniae on sputum Gram stain
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PORT INDEX PNEUMONIA SEVERITY INDEX FOR COMMUNITY-ACQUIRED PNEUMONIA(CAP)
Risk factor PointsDemographicsMen Age (years): Women Age (years) - 10: Nursing home resident +10
ComorbiditiesNeoplasm +30Liver disease +20Heart failure +10Stroke +10Renal failure +10
Physical examination findingsAltered mental status +20Respiratory rate ≥ 30 breaths per minute +20Systolic blood pressure < 90 mm Hg +20Temperature < 95˚F (35˚C) or ≥ 104˚F (40˚C) +15Pulse rate ≥ 125 beats per minute +10
Laboratory and radiographic findingsArterial pH < 7.35 +30Blood urea nitrogen > 30 mg per dL +20Sodium < 130 mmol per L +20Glucose ≥ 250 mg per dL +10Hematocrit < 30 percent +10Partial pressure of arterial oxygen < 60 mm Hg +10Pleural effusion +10Total points:
Pneumonia PORT severity index:
30-Day Mortality Date by Risk Class
Total Score
Risk Class
Recommended site of Therapy
Mortality range observed in validation
cohorts
None I Outpatient 0.1%
≤70 II Outpatient 0.6%
71-90 III Inpatient 0.9-2.8%
91-130 IV Inpatient 8.2-9.3%
>130 V Inpatient 27.0-29.2%
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Indikasi rawat inap
Skor PORT > 70Bila skor PORT < 70, penderita tetap di rawat
inap bila:– Frekuensi nafas > 30x/mnt– Pao2/ FiO2 kurang dari 250– Foto thoraks menunjukkan kelainan bilateral atau
lebih dari 2 lobus– Tekanan sistolik < 90 mmHg– Tekanan diastolik < 60 mmHg
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Treatment of CAP
HAP (Hospital Acquired Pneumonia/Nosocomial Pneumonia)/
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Diagnosa HAP/Hospital Diagnosa HAP/Hospital Acquired PneumoniaAcquired Pneumonia
ATS (American thoracic Society, 1996). Bila gejala ATS (American thoracic Society, 1996). Bila gejala pneumonia, terjadi pneumonia, terjadi 48-72 jam penderita masuk 48-72 jam penderita masuk rumah sakitrumah sakit, disebut HAP (dan diperkuat)dengan:, disebut HAP (dan diperkuat)dengan:
Infiltrat baru atau perubahan infiltrat selagi terjadi Infiltrat baru atau perubahan infiltrat selagi terjadi onset baruonset baru
Hipo/hipertermiHipo/hipertermi Produksi sputumProduksi sputum Lekositosis/lekopenia Lekositosis/lekopenia (Staufler, 1996)(Staufler, 1996)
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MANAGEMENTMANAGEMENT
Antibiotic therapy is the cornerstone of Antibiotic therapy is the cornerstone of treatment for both CAP and HAP.treatment for both CAP and HAP.
Initial therapy should be instituted rapidly.Initial therapy should be instituted rapidly.
Patients should initially be treated empirically, Patients should initially be treated empirically, based on the severity of disease and the likely based on the severity of disease and the likely pathogens.pathogens.
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Treatment of Early Onset Treatment of Early Onset HAPHAP
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Treatment of Late Onset Treatment of Late Onset HAPHAP
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Chronic Obstructive Pulmonary Disease
(COPD)
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 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
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Expanded View of Etiology, Pathogenesis and Pathology in
COPD
Expanded View of Etiology, Pathogenesis and Pathology in
COPD
Noxious stimulation
Chronic inflammation
Destruction, repair and remodeling
Abnormal function and symptoms
Asthma Is A Disease Of The Large & COPD The Small Airways
Asthma
Emphysema
Chronic Bronchitis
Chronic Bronchitis
trachea
bronchi
alveoli
Asthma Response
COPD Response
2 Agonist Bronchodilator Response
2 Agonist Bronchodilator Response
Anticholinergic
Panel A Panel B
COPD Pathology and Abnormal Breathing Mechanics
• ↑ Airway resistance • ↓ Elastic recoil • Expir. flow limitation• Air trapping and
dynamic hyperinflation• ↑ Work of breathing• Dyspnea, cough and
other respiratory • ↓ Quality of life
COPD - SIGNS
HYPERINFLATIONDECREASED EXPANSION CHESTPROLONGED EXPIRATION/±WHEEZESIGNS PULMONARY HYPERTENSION
AND/OR RVH (± CARDIAC FAILURE)CYANOSISHYPERCAPNIA - ASTERIXUS, (PRE)-
COMA
Look for pursed lip breathing or prolonged expiration
Tripod position suggests distress, resting weight on knees helps with chest expansion
MANAGING EXACERBATIONS(Emergency)(Emergency)
ANTIBIOTICS CONTROLLED OXYGEN BRONCHODILATOR - BETA AGONIST
ANTICHOLINERGIC, ±THEOPHYLLINE STEROIDS INTUBATION/VENTILATION TREAT HEART FAILURE IF PRESENT (RESPIRATORY STIMULANTS?)
BRONCHODILATORSFOR COPD
IPRATROPIUM BROMIDEOXITROPIUM BROMIDETIOTROPIUM BROMIDE
INHALEDANTICHOLINERGICS
,ANTIBIOTICS
IPRATOPRIUM BROMIDE&
SHORT ACTING INHALEDBETA 2 AGONIST
SHORT ACTING INHALED BETA 2 AGONIST
BETA 2AGONIST
COMBINATION
INHALER
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THEOPHYLLINE
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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).
CorticosteroidsCorticosteroids
• 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.
• 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.
Manage Exacerbations
Key Points
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).
• Inhaled bronchodilators (beta2-agonists and/or anticholinergics), theophylline, and systemic, preferably oral, glucocortico-steroids are effective for the treatment of COPD exacerbations (Evidence A).
AntibioticsAntibiotics• 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
• 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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Manage Exacerbations
Key Points
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).
•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).
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Acute Pulmonary Acute Pulmonary EdemaEdema
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DEFINISI EDEMA PARU
DEFINISI EDEMA PARU
• Terkumpulnya cairan ekstra vaskuler yg patologis di dalam paru(alveoli)
• Ok peningkatan tek.hidrostatik(Cardiogenic) atau tek.permeabilitas(Non Cardiogenic) pemb.darah kapiler paru.
• Terkumpulnya cairan ekstra vaskuler yg patologis di dalam paru(alveoli)
• Ok peningkatan tek.hidrostatik(Cardiogenic) atau tek.permeabilitas(Non Cardiogenic) pemb.darah kapiler paru.
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Microvascular fluid exchange in lung
Microvascular fluid exchange in lung
small gaps small gaps between between
endothelial cellsendothelial cells
tight tight junctionsjunctions
Peribronchovascular InterstitiumLymphatic Drainage
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Cause of acute pulmonary edema ?Cause of acute pulmonary edema ?Cause of acute pulmonary edema ?Cause of acute pulmonary edema ?
Cardiogenic pulmonary edema Hydrostatic or Hemodynamic edema
Non-cardiogenic pulmonary edema Increased-permeability pulmonary edema, acute lung
injury or acute respiratory distress syndrome
Difficult to distinguish because of similar Difficult to distinguish because of similar clinical manifestationsclinical manifestations
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DIFF.DIAGNOSIS OFPULMONARY EDEMADIFF.DIAGNOSIS OFPULMONARY EDEMA
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Pulmonary Edema: Pathophysiology
Pulmonary Edema: Pathophysiology
• A pathophysiologic condition, not a disease– Fluid in and around alveoli– Interferes with gas exchange– Increases work of breathing
• Two Types– Cardiogenic (high pressure)– Non-Cardiogenic (high permeability)
• A pathophysiologic condition, not a disease– Fluid in and around alveoli– Interferes with gas exchange– Increases work of breathing
• Two Types– Cardiogenic (high pressure)– Non-Cardiogenic (high permeability)
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Pulmonary EdemaPulmonary Edema
• High Pressure (cardiogenic)•AMI•Chronic HTN•Myocarditis
• High Permeability (non-cardiogenic)
•Poor perfusion, Shock, Hypoxemia•High Altitude, Drowning• Inhalation/infection of pulmonary
irritants
• High Pressure (cardiogenic)•AMI•Chronic HTN•Myocarditis
• High Permeability (non-cardiogenic)
•Poor perfusion, Shock, Hypoxemia•High Altitude, Drowning• Inhalation/infection of pulmonary
irritants
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Non-Cardiogenic Pulmonary Edema: Etiology
Non-Cardiogenic Pulmonary Edema: Etiology
• Toxic inhalation• Near drowning• Liver disease• Nutritional deficiencies• Lymphomas• High altitude pulmonary edema• Adult respiratory distress syndrome
• Toxic inhalation• Near drowning• Liver disease• Nutritional deficiencies• Lymphomas• High altitude pulmonary edema• Adult respiratory distress syndrome
Increased Permeability of Alveolar-Capillary Walls
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Pulmonary Edema: Signs &Symptoms
Pulmonary Edema: Signs &Symptoms
• Dyspnea on exertion• Paroxysmal nocturnal dyspnea• Orthopnea• Noisy, labored breathing• Restlessness, anxiety• Productive cough (frothy
sputum)/berbusa• Rales, wheezing• Tachypnea• Tachycardia
• Dyspnea on exertion• Paroxysmal nocturnal dyspnea• Orthopnea• Noisy, labored breathing• Restlessness, anxiety• Productive cough (frothy
sputum)/berbusa• Rales, wheezing• Tachypnea• Tachycardia
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Cardiogenic Pulmonary Edema: Etiology
Cardiogenic Pulmonary Edema: Etiology
• Left ventricular failure• Valvular heart disease
– Stenosis– Insufficiency
• Hypertensive crisis (high afterload)• Volume overload
• Left ventricular failure• Valvular heart disease
– Stenosis– Insufficiency
• Hypertensive crisis (high afterload)• Volume overload
Increased Pressure in Pulmonary Vascular Bed
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EVALUATION EVALUATION
天藍.地點:嘉義.攝影:杜漢祥
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HistoryHistoryHistoryHistory• Interstitial edema dyspnea and tachypnea• Alveolar flooding hypoxemia, cough & expectoration of
frothy edema fluid
• 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 associated with multiple blood-product transfusion
• Interstitial edema dyspnea and tachypnea• Alveolar flooding hypoxemia, cough & expectoration of
frothy edema fluid
• 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 associated with multiple blood-product transfusion
Unfortunately, the history is not always Unfortunately, the history is not always reliable.reliable.
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Pulmonary EdemaManagement
Pulmonary EdemaManagement
THE END
5858
Thanks for your attention!!Thanks for your attention!!