1

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

ASTHMA
BRONCHIALE

Asma- penyakit inflamasi kronik

Normal

Asma

Wall thickening
inflammation
-- mucus gland
hypertrophy

Bronchus

Secretions
Wall thickening
inflammation
repair
-- remodeling

Bronchiole

Loss of alveolar
attachments
Wall thinning inflammation elastolysis

Alveoli

Coalescence
Elasticity

2-Agonists

Virus?
Adenosine
Exercise
Fog

Antigen

BRONCHOCONSTRICTION
Mast cell
Macrophage

Airway smooth muscle

Eosinophil

AIRWAY
HYPERRESPONSIVENESS
Virus?
-lymphocyte

Reduction in Asthma
Attack
Improvement in the
control

Corticosteroids

PJ
of AsthmaBarnes
symptoms

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

corticosteroids on the pathophysiology of asthma.

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
7

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

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 beta 2-agonist

Current use of systemic

corticosteroids
or recent withdrawal from systemic
corticosteroids

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-agonist
every 60 minutes
Systemic corticosteroid
Continue treatment 1 to 3 hours,
provided there is improvement

Emergency Department and

Hospital Management: Treatment
After Repeat Assessment (continued)
FEV1 or PEF <50% predicted or personal
best
Physical exam: severe symptoms at rest,
accessory muscle use, chest retraction
History: high-risk patient
No improvement after initial treatment

Oxygen
Inhaled short-acting beta2-agonist
hourly or continuously + inhaled
anticholinergic
Systemic corticosteroid

Emergency Department and Hospital

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

Emergency Department and Hospital

Management:
Incomplete Response
FEV1 or PEF >50% but <70%
Mild-to-moderate symptoms

Individualized decision re:

hospitalization

Emergency Department and Hospital

Management:
Poor Response

FEV1 or PEF <50%

PCO2 >42 mm Hg
Physical exam: symptoms severe,
drowsiness, confusion

Admit to hospital intensive care

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

15

Step Up and Step Down Therapy of

Asthma
Outcome: Best
Possible Results

Outcome: Asthma Control

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)

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

Reliever: Rapid-acting inhaled 2-agonist prn

When
asthma is
controlled,
reduce
therapy

Monitor

STEP Down

16

PNEUMONIA
DEFINITION
Inflammation and consolidation of
lung
tissue due to an infectious agent
17

COMMUNITY
ACQUIRED (CAP)

Outpatiet

Inpatient

ICU

Typical

Atypical

HOSPITAL
ACQUIRED
(HAP)

18

19

PNEUMONIA/CAP
Merupakan infeksi saluran nafas bagian
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
20

Definition
Pneumonia is infection of the gas

exchanging (alveolar) compartment

of the lung (that is, it is a lower
respiratory tract infection)

(Bronchitis is infection of the

bronchial tree)
(Tracheitis or pharyngitis are
infections of the trachea or pharynx
respectively)
21

Pneumonia pathogenesis

22

 Pneumonia

in immunocompetent

patients
Community-acquired pneumonia
Hospital-acquired pneumonia (also

called nosocomial pneumonia)

Pneumonia

in
immunocompromised patients
23

Treatment of CAP

24

HAP (Hospital Acquired

Pneumonia/Nosocomial
Pneumonia)/

25

Diagnosa HAP/Hospital Acquired

Pneumonia)(Emergency)

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)
Oleh karena yang dirawat di ICU tidak selalu ada
gambaran diatas, dibuat penelitian klinis CPIS
(clinical pulmonary infection score)/VAP
26

MANAGEMENT

Antibiotic therapy is the cornerstone

treatment for both CAP and HAP.

of

Initial therapy should be instituted rapidly.

Patients should initially be treated empirically,

based on the severity of disease and the likely
pathogens.
27

Treatment of Early Onset

HAP

28

Treatment of Late Onset

HAP

29

Treatment of HAP:
Group 1

No risk factors for resistance+ mild-moderate presentation

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

Treatment of HAP: Group 2

Risk factors for resistance, and/or late onset + mildmoderate presentation (Contd)
Treatment:
3rd generation non-pseudomonal cephalosporin (eg.
ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV) or 4 th
generation cephalosporin (cefepime 1-2 g q12h IV)
OR
piperacillin-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 IV
31

HAP: Group 3-Severe Presentation (Hypotension, Need

for Intubation, Sepsis Syndrome, Rapid Progression of
Infiltrates or End Organ Dysfunction) and/or Risk for
Resistance

Treatment:

Treat with combination therapy :

anti-pseudomonal cephalosporin (ceftazidime or cefepime 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 g q8h IV)
plus
fluoroquinolone (ciprofloxacin 400 mg q8h IV or levofloxacin
750 mg q24h IV)
or
aminoglycoside (gentamicin or tobramycin 5-7mg/kg qd IV or
amikacin 15-20 mg/kg qd IV)
+/vancomycin 1 g q12 h IV or linezolid 600 mg q12 h IV if MRSA
present or suspected

32

Treatment of VAP: Group 4

No risk factors for resistance, early onset (<5 days
of hospitalization) & moderate presentation
Treatment:
3rd generation non-pseudomonal cephalosporin
(eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV)
or 4th generation cephalosporin (cefepime 2 g q12h
IV)
OR
beta-lactam/beta-lactamase inhibitor
(eg. piperacillin-tazobactam 4.5 g q6h IV)
OR
fluoroquinolone (levofloxacin 750 mg IV qd,
moxifloxacin 400 mg IV qd] po
33

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
PLUS
ciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IV
OR
gentamicin or tobramycin 5-7 mg/kg q24h IV or amikacin 1520 mg/kg q24h IV
+/vancomycin 1 g q12h IV or linezolid 600 mg q12h IV
34

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
36

COPD

Expanded View of Etiology,

Pathogenesis and Pathology in
COPD
Noxious
stimulation
Chronic
inflammation
Destruction,
repair and
remodeling
Abnormal
function and

CELLULAR MECHANISMS OF COPD

Cigarette smoke

Alveolar macrophage

CD8
lymphocyte
+

MCP-1

Neutrophil chemotactic factors

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

Neutrophil
PROTEASE
INHIBITORS

Neutrophil elastase
PROTEASES MatrixCathepsins
metalloproteinases

Alveolar wall destruction

(Emphysema)

Mucus hypersecretion
(Chronic bronchitis) 39

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

AND/OR RVH ( CARDIAC FAILURE)

CYANOSIS
HYPERCAPNIA - ASTERIXUS, (PRE)COMA

40

Expanded View of Etiology, Pathogenesis

and Pathology in COPD

Noxious stimulation
Chronic
inflammation
Destruction,
repair and
remodeling
Abnormal function
and symptoms

MANAGING
EXACERBATIONS
ANTIBIOTICS
CONTROLLED OXYGEN
BRONCHODILATOR - BETA AGONIST
ANTICHOLINERGIC,
THEOPHYLLINE
STEROIDS
NIV BIPAP
INTUBATION/VENTILATION
TREAT HEART FAILURE IF PRESENT
(RESPIRATORY STIMULANTS?)

1
INHALED
ANTICHOLINERGI
CS

IPRATROPIUM BROMIDE
OXITROPIUM BROMIDE
TIOTROPIUM BROMIDE

BRONCHODILATORS
FOR COPD
3

2
COMBINATIO
N
INHALER

BETA 2
AGONIST

SHORT ACTING INHALED

BETA 2 AGONIST

4
THEOPHYLLI
NE

IPRATOPRIUM BROMIDE
&
SHORT ACTING INHALED
BETA 2 AGONIST

Antibiotics
Acute exacerbations of COPD are

commonly assumed to be due to

bacterial infection, since they may be
associated with increased volume and
purulence of the sputum.
Exacerbations may be due to viral
infections of the upper respiratory tract
or may be noninfective, so that
antibiotic treatment is not always
warranted.
44

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
45

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).

46

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.

47

 Approximately 10 percent of

patients with stable COPD have

some symptomatic and objective
improvement with oral
corticosteroids. It is likely that
these patients have concomitant
asthma, since both diseases are
very common. Indeed, airway
hyperresponsiveness, a
characteristic of asthma, may
predict an accelerated decline in
FEV1 in patients with COPD.
48

 long-term treatment with high doses of

inhaled corticosteroids reduced the

progression of COPD, even when
treatment was started before the
disease became symptomatic.
Inhaled corticosteroids may slightly
reduce the severity of acute
exacerbations, but it is unlikely that
their use can be justified in view of the
risk of systemic side effects in these
susceptible patients and the expense of
using high-dose inhaled corticosteroids
for several years.
49

Manage
Exacerbations
Key Points

Exacerbations of respiratory
symptoms requiring medical
intervention are important clinical
events in COPD.
The most common causes of an
exacerbation are infection of the
tracheobronchial tree and air
pollution, but the cause of about
one-third of severe exacerbations
cannot be identified (Evidence B).

Manage
Exacerbations
Key Points
Inhaled bronchodilators (beta2agonists and/or anticholinergics),
theophylline, and systemic,
preferably oral, glucocorticosteroids are effective for the
treatment of COPD exacerbations
(Evidence A).

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).

Thanks for your attention!!

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