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KEGAWAT DARURATAN SISTEM PERNAPASAN (SERANGAN ASMA AKUT, PNEUMONIA DAN COPD) dan EDEMA PARU

ASTHMA

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Asma- penyakit inflamasi kronik
Normal Asma

Wall thickening – inflammation - mucus gland hypertrophy

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

Painting over rust

!!!
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European Respiratory Journal .Terapi Asma Masa Depan Asma Intermiten Persisten Tidak terkontrol LABACS Tidak terkontrol Tingkatkan dosis Boushey H. Is Asthma Control Achieveable ?. Dec 2004 Tujuan penatalaksanaan asma : TOTAL KONTROL Terkontrol Maintain Terkontrol .

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or For patients who fail to respond promptly and completely to an inhaled beta2-agonist 8 .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.

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 9 .

Risk Factors for Death From Asthma (continued)  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 .

Admit to Hospital Intensive Care • Inhaled beta2-agonist hourly or continuously + inhaled anticholinergic • IV corticosteroid • Oxygen • Possible intubation and mechanical ventilation • Admit to hospital ward 11 .

Step Up and Step Down Therapy of Asthma Outcome: Asthma Control Outcome: Best Possible Results Controller:  Controller: Controller: None  Controller: Daily inhaled corticosteroid    Daily inhaled corticosteroid Daily longacting inhaled β2-agonist  Daily inhaled corticosteroid Daily long – acting inhaled β2-agonist plus (if needed)  When asthma is controlled.agonist -Oral corticosteroid  Reliever: Rapid-acting inhaled β2-agonist prn STEP Down 12 . reduce therapy Monitor -Theophylline-SR -Leukotriene -Long-acting inhaled β2.

PNEUMONIA DEFINITION Inflammation and consolidation of lung tissue due to an infectious agent 13 .

COMMUNITY ACQUIRED (CAP) Outpatiet Typical Atypical Inpatient HOSPITAL ACQUIRED (HAP) ICU 14 .

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 • Seorang dokter umum(ugd) harus mampu mengenali dan mendiagnosis penyakit ini 15 .

or from aspiration or inhalation of chemicals or other toxic substances Risk factors: cigarette smoking. & immobility .organisms transmitted to lower airways and alveoli causing inflammation. fungus.impairs gas exchange Etiology: bacteria.   Inflammation & infection of lung.infecting organisms typically inhaled. virus. severe acute illness. Mycoplasma. suppressed immune system. chronic underlying disorders.

Pneumonia pathogenesis .

Klebsiella pneumoniae on sputum Gram stain 18 .Bacterial pneumonia.

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 < 95˚F (35˚C) or ≥ 104˚F (40˚C) 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 +30 +20 +10 +10 +10 +20 +20 +20 +15 +10 +30 +20 +20 +10 +10 +10 +10 19 .

0-29.2-9.2% 20 .1% 0.Pneumonia PORT severity index: 30-Day Mortality Date by Risk Class Total Score None ≤70 71-90 91-130 >130 Risk Class I II III IV V Recommended site of Therapy Outpatient Outpatient Inpatient Inpatient Inpatient Mortality range observed in validation cohorts 0.8% 8.3% 27.6% 0.9-2.

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 21 .Indikasi rawat inap  Skor PORT > 70  Bila skor PORT < 70.

Treatment of CAP 22 .

HAP (Hospital Acquired Pneumonia/Nosocomial Pneumonia)/ 23 .

terjadi 48-72 jam penderita masuk rumah sakit. disebut HAP (dan diperkuat)dengan:  Infiltrat baru atau perubahan infiltrat selagi terjadi onset baru  Hipo/hipertermi  Produksi sputum  Lekositosis/lekopenia (Staufler. 1996). 1996)  24 . Bila gejala pneumonia.Diagnosa HAP/Hospital Acquired Pneumonia ATS (American thoracic Society.

Initial therapy should be instituted rapidly. based on the severity of disease and the likely pathogens.MANAGEMENT  Antibiotic therapy is the cornerstone of treatment for both CAP and HAP.   25 . Patients should initially be treated empirically.

Treatment of Early Onset HAP 26 .

Treatment of Late Onset HAP 27 .

Ciliary cleansing mechanism of the respiratory tract is affected • Involves 3 diseases. air pollution.cigarette smoking. & Emphysema • Risk factors. allergens. occupational exposure. Also known as chronic airflow limitation (CAL) • Usually progressive & irreversible. stress 28 .Chronic Bronchitis. obstructive airflow diseases of the lungs. infections.Chronic Obstructive Pulmonary Disease (COPD) • A group of chronic. Asthma.

Pathogenesis and Pathology in COPD Noxious stimulation Chronic inflammation Destruction.Expanded View of Etiology. repair and remodeling Abnormal function and symptoms .

Asthma Is A Disease Of The Large & COPD The Small Airways Asthma Chronic Bronchitis trachea Emphysema bronchi Chronic Bronchitis alveoli .

2 Agonist Bronchodilator Response Anticholinergic Asthma Response Panel A COPD Response Panel B .

COPD Pathology and Abnormal Breathing Mechanics • • • • ↑ Airway resistance ↓ Elastic recoil Expir. cough and other respiratory • ↓ Quality of life . flow limitation Air trapping and dynamic hyperinflation • ↑ Work of breathing • Dyspnea.

ASTERIXUS.SIGNS  HYPERINFLATION  DECREASED EXPANSION CHEST  PROLONGED EXPIRATION/±WHEEZE  SIGNS PULMONARY HYPERTENSION AND/OR RVH (± CARDIAC FAILURE)  CYANOSIS  HYPERCAPNIA . (PRE)COMA .COPD .

Look for pursed lip breathing or prolonged expiration .

Tripod position suggests distress. resting weight on knees helps with chest expansion .

BETA AGONIST ANTICHOLINERGIC. ±THEOPHYLLINE  STEROIDS  INTUBATION/VENTILATION  TREAT HEART FAILURE IF PRESENT  (RESPIRATORY STIMULANTS?) .MANAGING EXACERBATIONS(Emergency)  ANTIBIOTICS  CONTROLLED OXYGEN  BRONCHODILATOR .

ANTIBIOTICS IPRATROPIUM BROMIDE OXITROPIUM BROMIDE TIOTROPIUM BROMIDE BRONCHODILATORS FOR COPD 3 2 BETA 2 AGONIST COMBINATION INHALER IPRATOPRIUM BROMIDE & SHORT ACTING INHALED BETA 2 AGONIST SHORT ACTING INHALED BETA 2 AGONIST 4 THEOPHYLLINE .1 INHALED ANTICHOLINERGICS.

<55 mm Hg).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. .

even at high doses. • However. • 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. the inflammation in COPD is not suppressed by inhaled or oral corticosteroids. .Corticosteroids • Inhaled corticosteroids are now the mainstay of therapy for chronic asthma.

glucocortico-steroids are effective for the treatment of COPD exacerbations (Evidence A).Manage Exacerbations Key Points • Inhaled bronchodilators (beta2-agonists and/or anticholinergics). theophylline. and systemic. . preferably oral.

• Although antibiotics are still widely used for exacerbations of 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. There is no evidence that prophylactic antibiotics prevent acute exacerbations 41 . methods to diagnose bacterial infection reliably in the respiratory tract are needed so that antibiotics are not used inappropriately.

increased volume and change of color of sputum. . and/or fever) may benefit from antibiotic treatment (Evidence B)..Manage Exacerbations Key Points • Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g.

Acute Pulmonary Edema 43 .

darah kapiler paru.DEFINISI EDEMA PARU • Terkumpulnya cairan ekstra vaskuler yg patologis di dalam paru(alveoli) • Ok peningkatan tek.permeabilitas(Non Cardiogenic) pemb.hidrostatik(Cardiogenic) atau tek. 44 .

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tight junctions small gaps between endothelial cells Microvascular fluid exchange in lung Peribronchovascular Lymphatic Interstitium Drainage 46 .

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 clinical manifestations 47 .

DIFF.DIAGNOSIS OF PULMONARY EDEMA 48 .

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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) 50 .Pulmonary Edema: Pathophysiology • A pathophysiologic condition.

Hypoxemia • High Altitude. Shock. Drowning • Inhalation/infection of pulmonary irritants 51 .Pulmonary Edema • High Pressure (cardiogenic) • AMI • Chronic HTN • Myocarditis • High Permeability (non-cardiogenic) • Poor perfusion.

Non-Cardiogenic Pulmonary Edema: Etiology • • • • • • • Toxic inhalation Near drowning Liver disease Nutritional deficiencies Lymphomas High altitude pulmonary edema Adult respiratory distress syndrome Increased Permeability of Alveolar-Capillary Walls 52 .

labored breathing Restlessness.Pulmonary Edema: Signs &Symptoms • • • • • • • • • Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthopnea Noisy. anxiety Productive cough (frothy sputum)/berbusa Rales. wheezing Tachypnea Tachycardia 53 .

Cardiogenic Pulmonary Edema: Etiology • Left ventricular failure • Valvular heart disease – Stenosis – Insufficiency • Hypertensive crisis (high afterload) • Volume overload Increased Pressure in Pulmonary Vascular Bed 54 .

EVALUATION 天藍.地點:嘉義.攝影:杜漢祥 55 .

trauma etc. Major trauma reliable. – Pneumonia. Focus on determining the the underlying clinical disorder history is not always • 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. Sepsis. associated with multiple blood-product transfusion 56 . Aspiration of gastric contents. cough & expectoration of frothy edema fluid •Unfortunately.History • Interstitial edema  dyspnea and tachypnea • Alveolar flooding  hypoxemia.

Pulmonary Edema Management THE END 57 .

Thanks for your attention!! 58 .

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