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

ASTHMA

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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Terapi Asma Masa Depan


Asma Intermiten Persisten
Tidak terkontrol LABACS Tidak terkontrol Tingkatkan dosis
Boushey H. Is Asthma Control Achieveable ?, European Respiratory Journal , Dec 2004

Tujuan penatalaksanaan asma : TOTAL KONTROL

Terkontrol

Maintain

Terkontrol

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 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

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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 2-agonist

Daily inhaled corticosteroid Daily long acting inhaled 2-agonist plus (if needed)

When asthma is controlled, reduce therapy Monitor

-Theophylline-SR -Leukotriene -Long-acting inhaled 2- agonist -Oral corticosteroid

Reliever: Rapid-acting inhaled 2-agonist prn

STEP Down

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

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COMMUNITY ACQUIRED (CAP)

Outpatiet

Typical

Atypical

Inpatient

HOSPITAL ACQUIRED (HAP)

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

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 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

+30 +20 +10 +10 +10

+20 +20 +20 +15 +10

+30 +20 +20 +10 +10 +10 +10

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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 0.1%


0.6% 0.9-2.8% 8.2-9.3% 27.0-29.2%
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Indikasi rawat inap


Skor PORT > 70
Bila 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

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HAP
(Hospital Acquired Pneumonia/Nosocomial Pneumonia)/

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Diagnosa HAP/Hospital Acquired Pneumonia


ATS (American thoracic Society, 1996). Bila gejala pneumonia, 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)

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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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Treatment of Early Onset HAP

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Treatment of Late Onset HAP

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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 28

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 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. flow limitation Air trapping and dynamic hyperinflation Work of breathing Dyspnea, cough and other respiratory Quality of life

COPD - SIGNS
HYPERINFLATION DECREASED EXPANSION CHEST PROLONGED EXPIRATION/WHEEZE SIGNS PULMONARY HYPERTENSION

AND/OR RVH ( CARDIAC FAILURE) CYANOSIS HYPERCAPNIA - 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)
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

BRONCHODILATORS FOR COPD


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2
BETA 2 AGONIST COMBINATION INHALER
IPRATOPRIUM BROMIDE & SHORT ACTING INHALED BETA 2 AGONIST

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.

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).

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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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).

Acute Pulmonary Edema

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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.

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tight junctions

small gaps between endothelial cells


Microvascular fluid exchange in lung

Peribronchovascular Interstitium Lymphatic Drainage


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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


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DIFF.DIAGNOSIS OF PULMONARY EDEMA

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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)

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Pulmonary Edema
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


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


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


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

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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.

associated with multiple blood-product transfusion

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Pulmonary Edema Management

THE END 57

Thanks for your attention!!


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