06 prof barmawi kegawatan asthma pneumonia copd

8/22/2019 06 Prof Barmawi Kegawatan Asthma Pneumonia Copd

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KEGAWAT DARURATAN

SISTEM PERNAPASAN(SERANGAN ASMA AKUT,

PNEUMONIA DAN COPD)

Blok Kegawatdaruratan, 26 Oktober 2011

[06]
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ASTHMA

BRONCHIALE

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Asma- penyakit inflamasi kronik

AsmaNormal


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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


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Antigen

2-Agonists

Corticosteroids

Virus?

Virus?

Adenosine

ExerciseFog

AIRWAY

HYPERRESPONSIVENESS

BRONCHOCONSTRICTION

Mast cell A i rway sm ooth musc le

Macrophage Eosinophi l

- lymphocyte

Barnes PJ

Complementary actions of long-acting b2-agonist(LABA) and

corticosteroids on the pathophysiology of asthma.

Reduction in Asthma Attack

Improvement in the control

of Asthma symptoms


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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 ICUfor asthma

Two or more hospitalizations for asthmain 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 canistersper month of inhaled

short-acting beta2-agonist

Current use of systemic corticosteroidsor recent withdrawal from systemic

corticosteroids


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Emergency Department and Hospital

Management: Treatment After Repeat

Assessment

FEV1 or PEF 50% to 80% predicted

or personal best

Physical exam: moderate

symptoms

Inhaled short-acting beta2-agonistevery 60 minutes

Systemic corticosteroid

Continue treatment 1 to 3 hours,

provided there is improvement


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Management: Treatment After Repeat

Assessment (continued) FEV1 or PEF


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Management:

Good Response

FEV1 or PEF >70%

Response sustained 60 minutes

after last treatment No distress

Physical exam: normal

Discharge Home

Distrss:bhya Sustd: trs mnerus


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Management:

Incomplete Response

FEV1

or PEF >50% but


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Management:

Poor Response

FEV1 or PEF 42 mm Hg

Physical exam: symptoms severe,drowsiness, confusion

Admit to hospital intensive care


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Admit to HospitalIntensive 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 ofAsthma

Reliever: Rapid-acting inhaled 2-agonist prn

Controller:

Daily inhaled

corticosteroid

Controller:

Daily inhaledcorticosteroid

Daily long-acting inhaled2-agonist

Controller:

Daily inhaled

corticosteroid Daily long

acting inhaled2-agonist

plus (if needed)

Whenasthma iscontrolled,reducetherapy

Monitor

STEP Down

Outcome: Asthma Control Outcome: BestPossible Results

Controller:

None-Theophylline-SR

-Leukotriene

-Long-acting inhaled

2- agonist-Oral corticosteroid


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PNEUMONIA

DEFINITION

Inflammation and consolidation of lung

tissue due to an infectious agent

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Outpatiet

Inpatient

ICU

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COMMUNITYACQUIRED (CAP)

HOSPITAL ACQUIRED

(HAP)

AtypicalTypical


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PNEUMONIA/CAP

Merupakan infeksi saluran nafas bagianbawah (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) harusmampu mengenali danmendiagnosis penyakit ini

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Definition

Pneumonia is infection of the gas exchanging(alveolar) compartment of the lung (that is, itis a lower respiratory tract infection)

(Bronchitis is infection of the bronchial tree)

(Tracheitis or pharyngitis are infections of the

trachea or pharynx respectively)

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Pneumonia pathogenesis

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Pneumonia in immunocompetentpatients

Community-acquired pneumonia

Hospital-acquired pneumonia (also callednosocomial pneumonia)

Pneumonia in immunocompromisedpatients

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T t t f CAP


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

pneumonia, terjadi 48-72 jam penderita masuk rumahsakit, disebut HAP (dan diperkuat)dengan:

Infiltrat baru atau perubahan infiltrat selagi terjadi onsetbaru

Hipo/hipertermi

Produksi sputum

Lekositosis/lekopenia (Staufler, 1996)

Oleh karena yang dirawat di ICU tidak selalu adagambaran diatas, dibuat penelitian klinis CPIS (clinicalpulmonary infection score)/VAP

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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, basedon the severity of disease and the likely pathogens.

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T t t f E l O t HAP


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Treatment of Early Onset HAP

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Treatment of Late Onset HAP

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Treatment of HAP:

Group 1 No risk factors for resistance+ mild-moderatepresentation

Treatment:

3rd generation non-pseudomonal cephalosporin(eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV)

or 4th generation cephalosporin (cefepime 1-2g

q12h IV)

OR

beta-lactam/beta-lactamase inhibitor

(eg. piperacillin-tazobactam 4.5 g q8h IV)

OR

fluoroquinolone (levofloxacin 750 mg IV qd or

moxifloxacin 400 mg IV qd) po 30


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Treatment of HAP: Group 2

Risk factors for resistance, and/or late onset + mild-

moderate presentation (Contd)

Treatment:3rd generation non-pseudomonal cephalosporin (eg.ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV) or 4th

generation cephalosporin (cefepime 1-2 g q12h IV)

ORpiperacillin-tazobactam 4.5 g q8h IV

OR

imipenem 500 mg q6h IV

OR

meropenem 500 mg q6h IV

OR

levofloxacin 750 mg q24h IV

OR

moxifloxacin 400 mg q24h IV

+/-

vancomycin 1 g q12h IV or linezolid 600 mg q12h IV31

HAP: Group 3-Severe Presentation (Hypotension, Need


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HAP: Group 3 Severe Presentation (Hypotension, Need

for Intubation, Sepsis Syndrome, Rapid Progression of

Infiltrates or End Organ Dysfunction) and/or Risk for

ResistanceTreatment:

Treat with combination therapy:anti-pseudomonal cephalosporin (ceftazidime orcefepime 2 g q8h IV)

or

beta-lactam/beta-lactamase inhibitor (piperacillin-tazobactam

4.5 g q6h IV)or

carbapenem (imipenem or meropenem 1g q8h IV or 1 gq8h IV)

plusfluoroquinolone (ciprofloxacin 400 mg q8h IV or

levofloxacin 750 mg q24h IV)or

aminoglycoside (gentamicin or tobramycin 5-7mg/kg qdIV or amikacin 15-20 mg/kg qd IV)

+/-

vancomycin 1 g q12 h IV or linezolid 600 mg q12 h IV ifMRSA present or suspected 32


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Treatment of VAP: Group 4

No risk factors for resistance, early onset (


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Treatment of VAP: Group 5

Risk factors for resistance present +/- severe presentation

Treatment:

ceftazidime 2 g q8h IV or cefepime 2g q8h IV

OR

imipenem-cilastatin 1 g q8h IV(ELASTYN)OR

meropenem 1 g q8h IV

OR

piperacillin-tazobactam 4.5 g q6h IV

PLUSciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IV

OR

gentamicin or tobramycin 5-7 mg/kg q24h IV or amikacin 15-20 mg/kg q24h IV

+/-

vancomycin 1 g q12h IV or linezolid 600 mg q12h IV

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Chronic Obstructive Pulmonary

Disease (COPD)

A group of chronic, obstructive airflow diseases of thelungs. Also known as chronic airflow limitation(CAL)

Usually progressive & irreversible; Ciliary cleansingmechanism 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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A group of chronic, obstructiveairflow diseases of the lungs. Alsoknown as chronic airflow limitation(CAL)

Usually progressive & irreversible;Ciliary cleansing mechanism of therespiratory tract is affected

Involves 3 diseases- Chronic

Bronchitis, Asthma, & Emphysema

Risk factors- cigarette smoking, airpollution, occupational exposure,infections, allergens, stress 36


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COPD


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Expanded View of Etiology, Pathogenesis

and Pathology in COPD

Noxiousstimulation

Chronic

inflammation

Destruction,

repair andremodeling

Abnormal function

and symptoms


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Cigarette smoke

Alveolar macrophage

Neutrophi l

PROTEASES

Alveolar wall destruction

(Emphysema)

Mucus hypersecretion

(Chronic bronchitis)

PROTEASEINHIBITORS

Neutrophil chemotactic factors

CELLULAR MECHANISMS OF COPD

Neutrophil elastaseCathepsins

Matrix metalloproteinases

Cytokines (IL-8)Mediators (LTB4)4 ))

?CD8+

l ymphocy te

-

MCP-1

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COPD - SIGNS

HYPERINFLATION

DECREASED EXPANSION CHEST

PROLONGED EXPIRATION/WHEEZESIGNS PULMONARY HYPERTENSION

AND/OR RVH ( CARDIAC FAILURE)

CYANOSIS

HYPERCAPNIA - ASTERIXUS, (PRE)-COMA

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E d d Vi f E i l P h i d


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Expanded View of Etiology, Pathogenesis and

Pathology in COPD

Noxious stimulation

Chronic

inflammation

Destruction,

repair and

remodeling

Abnormal function

and symptoms


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MANAGING

EXACERBATIONS

ANTIBIOTICS

CONTROLLED OXYGEN

BRONCHODILATOR - BETA AGONIST

ANTICHOLINERGIC, THEOPHYLLINE STEROIDS

NIV BIPAP

INTUBATION/VENTILATION

TREAT HEART FAILURE IF PRESENT

(RESPIRATORY STIMULANTS?)


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BRONCHODILATORS

FOR COPD

IPRATROPIUM BROMIDEOXITROPIUM BROMIDETIOTROPIUM BROMIDE

INHALEDANTICHOLINERGIC

S

IPRATOPRIUM BROMIDE&

SHORT ACTING INHALEDBETA 2 AGONIST

SHORT ACTING INHALEDBETA 2 AGONIST

BETA 2AGONIST

COMBINATIONINHALER

1

23

THEOPHYLLINE

4


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Antibiotics

Acute exacerbations of COPD are commonlyassumed to be due to bacterial infection, sincethey may be associated with increased volumeand purulence of the sputum.

Exacerbations may be due to viral infections ofthe upper respiratory tract or may benoninfective, so that antibiotic treatment is not

always warranted.

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Antibiotics

A meta-analysis of controlled trials of antibioticsin COPD showed a statistically significant butsmall benefit of antibiotics in terms of clinicaloutcome and lung function.

Although antibiotics are still widely used forexacerbations of COPD, methods to diagnosebacterial infection reliably in the respiratory tractare needed so that antibiotics are not used

inappropriately. There is no evidence thatprophylactic antibiotics prevent acuteexacerbations

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Oxygen

Long-term oxygen therapy:

reduced mortality

improvement in quality of life in patientswith severe COPD and chronic hypoxemia(partial pressure of arterial oxygen,


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Corticosteroids

Inhaled corticosteroids are now the mainstay oftherapy for chronic asthma,

However, the inflammation in COPD is not

suppressed by inhaled or oral corticosteroids, even athigh doses.

This lack of effect may be due to the fact thatcorticosteroids prolong the survival of neutrophils

and do not suppress neutrophilic inflammation inCOPD.

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Approximately 10 percent of patients withstable COPD have some symptomatic and

objective improvement with oralcorticosteroids. It is likely that thesepatients have concomitant asthma, sinceboth diseases are very common. Indeed,

airway hyperresponsiveness, acharacteristic of asthma, may predict anaccelerated decline in FEV1 in patients withCOPD.

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long-term treatment with high doses of inhaled

corticosteroids reduced the progression of COPD,even when treatment was started before thedisease became symptomatic.

Inhaled corticosteroids may slightly reduce the

severity of acute exacerbations, but it is unlikelythat their use can be justified in view of the risk ofsystemic side effects in these susceptible patientsand the expense of using high-dose inhaled

corticosteroids for several years.

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Manage Exacerbations

Key Points

Exacerbations of respiratory symptomsrequiring medical intervention are importantclinical events in COPD.

The most common causes of an exacerbationare infection of the tracheobronchial tree and

air pollution, but the cause of about one-third of severe exacerbations cannot beidentified (Evidence B).


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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).


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Key Points

Patients experiencing COPD

exacerbations with clinical signs of

airway infection (e.g., increased volumeand change of color of sputum, and/or

fever) may benefit from antibiotic

treatment (Evidence B).


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Thanks for your attention!!

06 prof barmawi kegawatan asthma pneumonia copd

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