STATUS ASTHMATICUS

Triwahju Astuti
ASTHMA PATHOGENESIS

Smooth muscle Airway

dysfunction inflammation

 Bronchoconstriction Inflammatory cell

  Bronchial hyper- infiltration/activation 
reactivity Mucosal oedema  
 Hyperplasia Cellular proliferation 
 Inflammatory Epithelial damage 
mediator release Basement membrane 
thickening

Symptoms\exacerbations
• Exacerbations of asthma (asthma attacks)
are episodes of a progressive increase in
shortness of breath, cough, wheezing, or
chest tightness, or a combination of these
symptoms.
 GINA 2006: ASSESS, TREAT AND MONITOR

Assessing Asthma Control

Treating to Achieve Control

Monitoring to Maintain Control

Key action steps in

new guidelines
GINA 2006
5 Components
Asthma Management & Prevention

1. Develop Patient/Doctor Partnership

2. Identify and Reduce Exposure to Risk
Factors
3. Assess, Treat, and Monitor Asthma
4. Manage Asthma Exacerbation
5. Special Considerations
GINA 2006
KLASIFIKASI SERANGAN ASMA

• RINGAN
• SEDANG
• BERAT
• MENGANCAM JIWA

6
GINA 2009

Severity of Asthma Exacerbations…..

MILD MODERATE SEVERE RESPIRATORY
ARREST
IMMINENT

Breathless Walking Talking At rest

Infants – softer Infants- Stops
shorter cry feeding
Can lie flat Prefers sitting *Hunched forward

Talks in Sentences Phrases Words

Alertness May be agitated Usually agitated Usually agitated

Respiratory Rate Increased Increased *Often >30/min Bradypnea

GUIDE TO RATES OF BREATHING ASSOCIATED WITH

RESPIRATORY DISTRESS IN AWAKE CHILDREN
AGE NORMAL RATE
> 2 months < 60/min
2-12 months < 50/min
1-5 years < 40/min
6-8 years < 30/min 7
GINA 2009

Severity of Asthma Exacerbations…..

MILD MODERATE SEVERE RESPIRATORY

ARREST IMMINENT

Accessory None Present Present Present

Muscles & Thoraco-abdominal
Suprasternal Movement
Retraction

Wheeze Audible with Audible with Audible w/o Absence of wheeze

stethoscope stethoscope stethoscope with decreased to
absent breathe sounds

Pulses/min <100 100-120 >120 Bradycardia

GUIDE TO LIMITS OF NORMAL PULSE RATE IN CHILDREN

Age Normal Limits
Infants 2-12 months <160/min
Preschool 1-2 years <120/min
School Age 2-6 years <110/min 8
GINA 2009
Severity of Asthma Exacerbations
MILD MODERATE SEVERE RESPIRATORY
ARREST
IMMINENT

Pulses Paradoxus Absent May be present Often present Absence suggests

<10mm Hg 10—20mm Hg 20-40mm Hg respiratory muscle
fatigue

PEF  80% 60-79% <60%

%predicted
Or
%personal best

PaO2 RA Normal 60mm Hg <60mmHg

test NOT usually Possible Cyanosis
necessary

PaCO2 45 mm Hg 45 mm Hg >45 mm Hg possible

respiratory failure

SaO2 RA 95% 90-94% <90%

9
 TUJUAN PENATALAKSANAAN
PADA EKSASERBASI AKUT

 Menghilangkan obstruksi secepat mungkin

 Menghilangkan hipoksemi

 Mengembalikan faal paru ke normal secepat

mungkin

 Mencegah kekambuhan

Perhimpunan Dokter Paru Indonesia Diagnosis dan Penatalaksanaan Asma dari PDPI dan
(The Indonesia Society of Respirology) Implementasi GINA di Indonesia
CORTICOSTEROID / LONG ACTING BETA-2 AGONIST (LABA)

Smooth muscle Airway

LABA dysfunction inflammation
Corticosteroid

 Bronchoconstriction Inflammatory cell

  Bronchial hyper- infiltration/activation 
reactivity Mucosal oedema  
 Hyperplasia Cellular proliferation 
 Inflammatory Epithelial damage 
mediator release Basement membrane 
thickening

Symptoms\exacerbations
HIGH RISK OF ASTHMA-RELATED DEATH :

• History of near-fatal asthma requiring intubation &

mechanical ventilation
• Hospitalization or emergency visit for asthma within the
past year
• Currently using or have recently stopped using oral
glucocorticosteroids
• Not currently using inhaled glucocorticosteroids
• Overdependent on rapid-acting inhaled 2-agnoists,
especially those who use more than one canister of
salbutamol (or equivalent) monthly
• History of psychiatric disease or psychosocial problems,
including the use of sedatives
• History of noncompliance with an asthma medication plan
 ASTHMA ATTACKS REQUIRE PROMPT TREATMENT:

• Inhaled rapid-acting 2-agonists in adequate doses are

essential. (Begin with 2 to 4 puffs every 20 minutes for the
first hour; then Moderate exacerbations 6 to 10 puffs every
1 to 2 hours; Mild exacerbations will require 2 to 4 puffs
every 3 to 4 hours.)

• Oral glucocorticosteroids (0.5 to 1 mg of prednisolone/kg or

equivalent during a 24-hour period) introduced early in the
course of a moderate or severe attack help to reverse the
inflammation & speed recovery.
•
• Oxygen is given at health centers or hospitals if the patient
is hypoxemic (achieve O2 saturation of 95%).
• Combination 2-agonist/anticholinergic therapy is
associated with lower hospitalization rates & greater
improvement in PEF and FEV1.
• Methylxanthines are not recommended if used in addition
to high doses of inhaled 2-agonists. However, theophylline
can be used if inhaled 2-agonists are not available. If
the patient is already taking theophylline on a daily basis,
serum concentration should be measured before adding
short-acting theophylline.
THERAPIES NOT RECOMMENDED FOR TREATING ASTHMA
ATTACKS INCLUDE:
• Sedatives (strictly avoid)
• Mucolytic drugs (may worsen cough)
• Chest physical therapy/physiotherapy (may increase patient
discomfort)
• Hydration with large volumes of fluid for adults & older
children (maybe necessary for younger children & infants)
• Antibiotics (do not treat attacks but are indicated for patients
who also have pneumonia or bacterial infection such as
sinusitis)
• Epinephrine/adrenaline (may be indicated for acute
treatment of anaphylaxis & angioedema but is not indicated
for asthma attacks)
MONITOR RESPONSE TO TREATMENT:

• Evaluate symptoms and, as much as possible, peak

flow.
• In the hospital also assess oxygen saturation;
consider arterial blood gas measurement in patients
with suspected hypoventilation, exhaustion, severe
distress, or peak flow 30-50 percent predicted.
FOLLOW UP:

• After the exacerbation is resolved, the

factors that precipitated the exacerbation
should be identified and strategies for their
future avoidance implemented, and the
patient’s medication plan reviewed.
PENANGANAN ASMA EKSASERBASI
DI RUMAH SAKIT
Penilaian Awal
Anamnesis, PF ( penggunaan otot bantu napas, denyut
jantung, frekuensi napas, auskultasi)
APE atau VEP1 , saturasi oksigen, dan tes lain yang diperlukan

Terapi Awal
• Inhalasi 2-agonis kerja cepat secara terus menerus selama 1 jam.
• Oksigen sampai tercapai saturasi O2 > 90% (95% pada anak-anak)
• Steroid sistemik jika tidak ada respons segera, atau jika pasien
sebelumnya sudah menggunakan steroid oral atau jika derajat
keparahan sudah berat
• Sedasi merupakan kontra-indikasi terapi asma eksaserbasi.

Penilaian Ulang setelah 1 jam

APE, saturasi O2, tes lain yang diperlukan
Ref. GINA Updated18
2008
lanjutan ….
Penilaian Ulang stlh 1 jam

Derajat Sedang Derajat Berat

APE 60-80% dari yang diperkirakan
•Pem. Fisik : gejala sedang,
penggunaan otot bantu pernapasan
•Oksigen
•Inhalasi 2-agonis dan anti-
kolinergik setiap 60 menit
•Glukokortikosteroid oral
•Teruskan terapi 1-3 jam jika ada
perbaikan
Penilaian Ulang stlh 1-2 jam
•APE < 60% dari yang diperkirakan
•PF: gejala berat saat istirahat, retraksi
dada
•Riwayat faktor resiko mendekati
asma yang fatal
•Tidak ada perbaikan setelah terapi
awal
•Inhalasi 2 -agonis dan anti-kolinergik
•Oksigen
•Glukokortikosteroid sistemik
•Magnesium IV

Respons tidak baik Respons buruk

Respons baik
selama 1-2 jam selama 1-2 jam

Ref. GINA Updated19

2008
 Respons Baik Respons tidak lengkap Respons jelek
• Bertahan 60 menit setelah selama 1-2 jam selama 1 jam
terapi terakhir • Pasien resiko tinggi • Pasien resiko tinggi
• PF : normal • PF: gejala ringan-sedang • PF: gejala berat, kesadaran
• APE > 70% • APE < 70% menurun, kebingungan
• Tidak stres • Saturasi O2 tidak membaik • APE < 30%
• Saturasi O2 > 90% • PCO2 > 45mm Hg
(95% pada anak-anak) • PO2 < 60mm Hg

Pulangkan ke Rumah Rawat Rumah Sakit Rawat di ICU

• Lanjutkan 2-agonis inhalasi
• Pertimbangkan steroid oral
• Pertimbangkan inhaler kombinasi
• Edukasi pasien:
Cara pakai obat yang benar
Buat rencana aksi
Follow-up teratur
(acute care setting)
• Inh 2-agonis ± anti-kolinergik
• Steroid sistemik
• Oksigen
• Magnesium IV
• Monitor APE, saturasi O2 , nadi
• Inh b2-agonis + anti-kolinergik
• Steroid IV
• Pertimbangkan 2 -agonis IV
• Oksigen
• Pertimbangkan teofilin IV
• Intubasi dan ventilasi mekanik
jika perlu

Kriteria bisa dipulangkan Perbaikan Tidak membaik Rawat di ICU

• jika APE > 60% dari yang
diperkirakan Jika tidak ada perbaikan
• Kondisi tetap pada saat terapi setelah 6-12 jam
oral / inhalasi

Ref. GINA Updated20

2008
KLASIFIKASI ASMA EKSASERBASI
 COMPARISON EFFECTS OF TERBUTALINE NEBULISATION AND
SUBCUTANEOUS ADRENALIN IN ACUTE ASTHMA

200

150

100
terbutaline

50 Adrenalin

0
A 15 30 60 120 240

Rai IBN. Dept. of Pulmonologi FKUI, 1986

 COMPARISON EFFECTS OF NEBULIZATION AND INTRAVENOUS
SALBUTAMOL IN ACUTE ASTHMA
PFR (l/menit)
300

250

200

150 V
H
100

50

0
0 15 30 45 60 75 90 105 120
Katili AM, dkk. Med J Indones 1995;4:264-73
 STATUS ASTHMATICUS

A life-threatening form of asthma in which

progressively worsening reactive airways are
unresponsive to usual appropriate therapy that
leads to pulmonary insufficiency.
 PATHOPHYSIOLOGY

• Reversible, recurrent, diffuse obstructive pulmonary

disease process caused by airway inflammation & hyper-
reactivity.The primary pathophysiology includes:
• Smooth muscle spasm
• Mucosal edema
• Mucous plugging.
• These changes in the airway cause airflow obstruction
leading to premature airway closure on expiration which
causes hypercarbia & dynamic hyperinflation. This
dynamic hyperinflation or “air-trapping”  ventilation /
perfusion (V/Q) mismatching causing hypoxemia.
MEKANISME EKSASERBASI

Murray CS, Simpson A and Custovic A, 2004. Allergens, viruses, and asthma exacerbations.
Proc Am Thorac Soc. 1:99-104.
Adapted and reprinted from The Lancet, 368, Holgate ST, Polosa R. The mechanisms, diagnosis, and
management of severe asthma in adults, 780–93. Copyright (2006), with permission from Elsevier. 27
 CLINICAL PRESENTATION
• SA patients may be unresponsive to treatment, have
minimal respiratory reserve & have a deteriorating clinical
condition. Upper respiratory tract infections are often
found
• The presence or absence of wheezing while examining a
child with SA requires special attention. The clinical exam
of wheezing changes as the disease progresses:
- Expiratory wheeze: airways only obstruct during
expiration
- Inspiratory and expiratory wheeze: airways are
obstructed throughout the respiratory cycle
- Little air movement heard (“tight”): complete airway
obstruction occurs despite maximal patient
effort suggesting impending respiratory failure
• Other exam findings that signify severe respiratory
function compromise include:
• Retractions
• Prolonged expiratory phase
• Pulsus paradoxus - systolic blood pressure drop of
more than 18 mmHg with inspiration in
teenagers or more than 10 mmHg in children
• Evidence of cyanosis/hypoxemia - PaO2 less than
60mmHg, change in consciousness
• Hypercapnia - PaCO2 greater than 40mmHg in
presence of dyspnea and wheezing
• Metabolic acidosis
• FEV1 or PEFR (peak expiratory flow rate) less
than 20% predicted with little or no
response to acute therapy
 DIAGNOSTICS
• A chest radiograph  to define the extent of the associated
parenchymal disease and to rule out other diagnoses (e.g.
foreign body, infiltrate). Hyperinflation and peribronchial
thickening are common findings.
• Laboratory tests to evaluate the degree of acidosis and for a
potential infection are beneficial.
• Spirometry  assess severity of disease. A fall in FEV1 has
been shown to correlate well with the degree of airway
obstruction and hypoxemia in status asthmaticus.
• Blood gases:  in asthma management, they should not be
used to determine the need for intubation.The patient’s
clinical status should be the grounds for intubation
 TREATMENT

• Intravenous Fluids: inevitably dehydrated due to

poor oral intake, tachypnea, and often emesis.
The dehydration often causes a metabolic
acidosis as well increasing their work of
breathing. Rehydration prevents thickening of
mucous secretions and begins to treat the
metabolic acidosis.
• Albuterol: first line therapy
• Mechanism of action: a β2 agonist
responsible for smooth muscle relaxation
• Dosing: Continuous nebulization - 10-20
mg/hr (or 0.5-0.6 mg/kg/hour) with an
oxygen flow rate of 10 – 12L/min
• Advantages: rapid acting and can be rapidly
administered
• Disadvantages: tachycardia, hyperglycemia,
hypokalemia.
• Other: Nebulization is preferred to MDI
 IPRATROPIUM BROMIDE (ATROVENT):
• Mechanism of action: anticholinergic, muscarinic –
M1, receptors mediate bronchoconstriction
• Dosing: 0.25 – 0.5 mg nebulized
o Q20 min X 3 doses with continuous albuterol
has proven effective in acute management
o Every 6- 8 hrs with Albuterol for chronic
treatment
• Advantages: has no systemic anticholinergic action
• Other: unilateral pupillary dilation can occur with local
med entry
CORTICOSTEROIDS – SOLU-MEDROL
• Mechanism of action: effective in controlling
or preventing the sustained inflammatory phase
which occurs 6-8 hours after allergen exposure
• Dosing: Methyl-prednisone
o Loading dose: 2 mg/kg IV
o Maintenance dose: 0.5mg/kg IV q 6hr
• Other: Steroids should be administered IV to
SA patients to assure adequate drug delivery in
a timely manner. Given the risk of emesis
and differential absorption enterally, the
drug should not be administered orally.
 MAGNESIUM SULFATE
• Mechanism of action: smooth muscle relaxant
• Dosing: 50 mg/kg IV over 20 min with max of 2 gm
• Advantages: has been shown to be effective in “severe”
(FEV1<25% predicted) asthma
• Disadvantages / Side effects: rarely noted; hypotension,
respiratory depression & muscle weakness can be
treated with IV Calcium Gluconate
• Other: respiratory depression & muscle weakness are noted
only at levels >12mg/dL. Normal Mg levels are 1.5-
2mg/dL and minimal increase in level is noted with a
single dose of magnesium. Therefore, there should be
little concern by the practitioner of causing respiratory
depression with a single dose of magnesium sulfate.
 TERBUTALINE
• Mechanism of action: IV β2 agonist
• Dosing:
o Loading dose: 5 - 10mcg/kg IV over 10 min
o Continuous infusion: 0.4 - 4 mcg/kg/min IV
• Advantages: effectively reaches areas of lung by
intravenous infusion that Albuterol does not due to
airway obstruction
• Disadvantages / side effects: tachycardia, hyperglycemia,
hypokalemia, (rhabdomyolysis & cardiac ischemia –
rarely)
• Other: the continuous infusion can be increased every 20-
30 minutes by 0.4mcg/kg/min until the patient’s
symptoms begin to subside.
 AMINOPHYLLINE
• Mechanism of action: phosphodiesterase inhibitor which
allows for smooth muscle relaxation and augments
mucociliary clearance
• Dosing:
o Loading dose: 6 mg/kg over 20 min IV
o Continuous infusion: 0.6 - 1 mg/kg/min IV
• Advantages: may prove very effective in patients resistant
to above treatments given the different
mechanism of action
• Disadvantages / side effects: nausea, vomiting, agitation,
arrhythmias, seizures
• Other: A theophylline level needs to be checked 8 hours
after drug initiation and then every morning.
Therapeutic levels are 10 – 20 mcg/ml.
 HELIOX
• Mechanism of action: It is a low-density gas that increases
laminar flow and decreases turbulent flow. can be used
concomitantly with Albuterol (may improve delivery), and
may be given in intubated or non-intubated patients.
• Dosing: only effective with 60% or greater helium. Patients
requiring greater than 40% FiO2 cannot be placed on heliox.
• Advantages: has no systemic side effects (except causing
high pitched voice)
• Other: The data to date is not conclusive, but small studies
have shown both objective and subjective improvements in
patients receiving heliox along with the prevention of
intubation. In intubated patients, heliox has been shown to
decrease the PIP requirements.
 MECHANICAL VENTILATION
The two primary indications to intubate an SA patient are:
• Severe hypoxia
• Depressed level of consciousness
Other potential indications for mechanical ventilation include:
• Obvious life-threatening respiratory distress not responding
to bronchodilator therapy – impending respiratory failure
• Hemodynamic compromise, including bradycardia, severe
pulsus paradoxus
• Lactic acidosis associated with increased work of breathing
• Apnea or near-apnea
• Peak flows <40% of predicted
The decision to intubate a patient with asthma should not be
taken lightly since:
1) patients are at risk for severe decompensation
during intubation
2) mechanical ventilation doesn’t directly help with
expiration (which is the primary problem in a
patient with status asthmaticus)
Potential complications include:
• Pneumothorax / tension pneumothorax –
introduction of positive pressure into hyper-inflated
lungs, i.e. air-trapping
• Hemodynamic instability – since they are often
volume depleted