1

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

ASTHMA

2

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

5

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

8

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

9

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

11

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

12

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

13

Outpatiet

Inpatient

ICU

Outpatiet

Inpatient

ICU

14

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

15

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

18

19

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%

20

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

21

22

Treatment of CAP

HAP (Hospital Acquired Pneumonia/Nosocomial Pneumonia)/

23

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)

2424

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.

2525

Treatment of Early Onset Treatment of Early Onset HAPHAP

2626

Treatment of Late Onset Treatment of Late Onset HAPHAP

2727

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

28

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

1

23

THEOPHYLLINE

4

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

41

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).

43

Acute Pulmonary Acute Pulmonary EdemaEdema

44

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.

45

46

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

47

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

48

DIFF.DIAGNOSIS OFPULMONARY EDEMADIFF.DIAGNOSIS OFPULMONARY EDEMA

49

50

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)

51

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

52

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

53

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

54

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

55

EVALUATION EVALUATION

天藍．地點：嘉義．攝影：杜漢祥

56

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.

57

Pulmonary EdemaManagement

Pulmonary EdemaManagement

THE END

5858

Thanks for your attention!!Thanks for your attention!!