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MANAGEMENT OF

ASTHMA ACUTE ATTACK


(Status Asthmaticus)
Dadang Hudaya Somasetia
Pediatric Emergency/Pediatric ICU
Hasan Sadikin General Hospital
Dept of Child Health - Faculty of Medicine
Padjadjaran University Bandung

Definition
Asthma: Diffuse pulmonary disease
characterized by hyper-reactivity of trachea
and bronchi, causing generalized narrowing
of the airway in response to certain
nonspecific stimuli.
Status asthmaticus: Life threatening form of
asthma characterized by unresponsiveness
to the usual adrenergic drugs, resulting in
respiratory failure.

Asthma Acute Attack


Asthma

Affects 10% of children


Causes 25% of school absenteeism
Hospitalization rate has tripled
Death rate has increased in last 15 years
Accounts for 5% of PICU admissions

STATUS ASTHMATICUS:
Asthma attack refractory to initial therapy

Asthma Acute Attack


Etiology/Pathology for Asthma

Bronchial Muscle Spasm


Mucosal Edema
Thick Mucus Secretion

Asthma Acute Attack


Clinical Findings for Asthma

Wheezing
Tachypnea
Retractions
Nasal flaring
Use of accessory
muscles

Cough
Anxiety
Dehydration
Tachycardia
Late bradypnea

Asthma Acute Attack


Interventions for Asthma

Oxygen
Beta2-agonist bronchodilator
Consider steroids
Medications
Consider mechanical ventilation

PULMONARY SCORE for ASTHMA ACUTE ATTACK


SCORE Respiratory Rate
< 6 yr
> 6 yr

Wheeze

Accessory muscle use


(Sternocleidomastoideus)

< 30

< 20

None

No apparent activity

31-45

21-35

Terminal expiration
heard with
stethoscope

Questionable increase

46-60

36-50

Entire expiration
heard by
stethoscope

Increase apparent

> 60

> 50

inspiration and
expiration
without stethoscope

Maximal activity

If no wheezing due to minimal air exchange, score 3


Score < 3 = mild, 4-6 = moderate, > 6 = severe

Indicators of Severe Asthma


Anxious

& diaphoretic appearance, upright position

Breathlessness
PaCO2

at rest and inability to speak in full sentences

normal or increased

PEFR

< 150 L/min or <50% predicted

Pulse

oximetry < 91% on room air

Tachycardia

(HR>120) and tachypnea (RR>30)

Expert Panel Report 2: Guidelines for the diagnosis and management of asthma.
National Institute of Health- National Heart, Lung and Blood Institute 1997; NIH
publication number 97-4051

Approach to Severe Asthma


Reverse

bronchoconstriction
Treat airway inflammation
Correct hypoxemia
Consider differential
diagnosis
Monitor for complications
Pneumothorax
Hypotension

Mild Exacerbation (Schuch et al. J pediatr 1995;126:639-45)


2 Agonist
2 Agonist + ipratropium bromide

Severe Exacerbation (KNAA Updated 2002)

2 Agonist + ipratropium bromide

Insufficient response systemic corticosteroid


To reduced oral systemic corticosteroid in frequent episodic
high doses budesonide inhalation
(2mg every 8 hours)
Acta paediatr 1999;88:841-3

Asthma Acute Attack


Asthma: Common Failures of Management

Underestimating severity of symptoms


Lack of dynamic observation
Underuse of beta-agonists and steroids
Instituting mechanical ventilation after arrest, not
before

In the management of a severe


asthma exacerbation
How

should beta-agonists be
administered?
Do anti-cholinergics have a role?
Does aminophylline have a role?
Does magnesium have a role?
Should heliox be used?
Does ketamine have a role?
Should non-invasive ventilation be used?
What should the ventilator settings be if
the patient is intubated?

If the patient is unable to tolerate


inhaled -agonists

SC

-agonists are an alternative to inhaled -agonists

A randomized

trial compared SC epinephrine 0.3-0.5


mg with SC terbutaline 0.25-0.5 mg
Patients
Similar
No

18-64 years old

increases in PEFR and FEV at 5 and 15 minutes

difference in heart rate or blood pressure

Continuous

ECG revealed no dysrhythmias

Spiteri: Subcutaneous adrenaline versus terbutaline in the treatment of acute


severe asthma. Thorax 1988; 43:19-23

Should IV -agonist therapy be used?


Meta-analysis

evaluated 9 RCTs comparing IV


-agonists in addition to, or instead of,
inhaled -agonists in severe asthma in adults
No significant differences were found in
multiple outcome measures between the two
groups
If the patient can tolerate inhaled -agonists,
there is no evidence to support the use of IV
-agonists
Travers et al. The Cochrane Library, Issue 3, 2003.

trial found a benefit of IV -agonists in


children

Small

Browne et al. Lancet 1997; 349: 301-305.

All patients with a severe asthma


exacerbation should receive steroids
60

125 mg IV methylprednisolone
40-60 mg PO prednisone
(2 mg/kg)

Should anticholinergics be used in


addition to -agonists?
Multiple

doses of inhaled ipratropium bromide


in addition to -agonists lead to a significant
improvement in pulmonary function tests
Benefits most pronounced in those with
FEV1<30%
Rodrigo. The Role of Anticholinergics in Acute Asthma
Treatment- An Evidence-Based evaluation. Chest 2002;
121.1977-87.

Is there a role for IV aminophylline?


Multiple

theoretically beneficial effects


Cochrane review included 15 trials and found no
benefit over -agonists alone in PFTs or admission
rates, even in severe asthma
Increase in adverse effects (palpitations, vomiting)
Parameswaran et al. The Cochrane Library, Issue 3, 2003

No

studies compare outcome in patients with


severe asthma who are unable to tolerate inhaled
-agonists
There is no evidence supporting its use

Is there a role for IV


magnesium?
Smooth

muscle relaxation
(bronchodilation)
2 gm of MgSO4 is safe and beneficial
in patients with severe acute asthma
exacerbations (FEV1<25% predicted)
Rowe. Magnesium sulfate for treating exacerbations of
acute asthma in the emergency room (Cochrane Review)
The Cochrane Library. Issue 3, 2003.

25-50

mg/kg max 2 gm

What is heliox?
Helium/Oxygen
Laminar

mixture

flow reduces the resistance

associated turbulent airflow in more


proximal airways
Allows

greater oxygen delivery during

inspiration
Reduced

work of breathing

Should heliox be used in severe


asthma?
Review

found no improvement in PFTs


regardless of heliox mixture or severity of
disease

Heliox-driven

nebulizers were associated with


a non-significant improvement in PFTs at one
hour
Rodrigo. Chest 2003; 123: 891-896.
Rodrigo. The Cochrane Library. Issue 3, 2003

Does IV ketamine improve


outcome?
Ketamine

is a bronchodilator, potentiates catecholamines


44 consecutive patients with severe asthma attacks
received IV ketamine (0.1 mg/kg bolus and 0.5
mg/kg/hour infusion) for 3 hours
Ketamine was used in conjunction with other standard
therapies
No difference in PEFR or hospital admission
Howton. Randomized, double-blind, placebo-controlled trial of IV ketamine in acute asthma.
Annals of Emergency Medicine. 27(2). 1996.

Does noninvasive ventilation improve outcome?


BiPAP

can reduce work of breathing, reduce


bronchoconstriction and offset intrinsic PEEP
Small trial used BiPAP in 30 patients with
severe asthma after one neb in the ED
Excluded patients with hypotension, Osat <
90%, depressed mental status, need for
emergent intubation
BiPAP was interrupted for short periods to
deliver nebulized albuterol
Significant improvement in PFTs
Soroksky et al. A Pilot Prospective, RCT of BiPAP in Acute Asthma
Attack. Chest 2003. 123: 1018-1025.

Asthma Acute Attack


Asthma: Intubation Issues

Intubation may worsen bronchospasm


BP may fall with intubation due to hypovolemia and
cardiopulmonary interactions
Severe hypoxia can occur despite optimal rapid
sequence induction technique
Bag-mask or bag-ET ventilation will be difficult due to
the airway pressure required
Pneumothorax risk increases after intubation

Asthma Acute Attack


Asthma: Relative Intubation Criteria

Deterioration in state of consciousness with inability


to protect the airway
Apnea or near apnea
Hypoxemia refractory to maximal FiO2

Who should be intubated?


Decision

should be based on
clinical deterioration (altered mental
status, respiratory fatigue)

Neither

hypoxia nor hypercarbia


are absolute indications for
intubation

Do

not wait until respiratory arrest!

Rapid Sequence Intubation in the


Asthmatic
Oxygenate
Premedicate

Lidocaine
Glycopyrollate or atropine

Induction

with ketamine

Paralysis

with succinylcholine

Intubation

with large ETT

Mechanical Ventilation in
Asthma
Volume

cycled ventilation
FiO2
1.0
Rate
8-10
I:E 1:4 or 1:5
VT 5-7 cc/kg
PEEP 0
Maintain
peak pressures < 45 cm H20,
plateau pressure < 30 cm H20

If peak pressures remain > 45 mm Hg


Evaluate
Ensure
Allow

for pneumothorax

sedation & paralysis

hypercapnea (up to 80 mmHg)

Consider

pressure-controlled

ventilation

Complications of Mechanical
Ventilation
Hypotension
Barotrauma

Asthma Acute Attack


Asthma: Referral to a CRPC

Post-arrest with or
without intubation
Failure to improve after
intensive ED Rx
Air leak syndrome
Clinical dehydration or
risk of dehydration

Altered

LOC
Exhaustion
Deteriorating patient
Drug toxicity
Silent chest

Asthma Acute Attack


Asthma: Common Failures of Management

Underestimating severity of symptoms


Lack of dynamic observation
Underuse of beta-agonists and steroids
Instituting mechanical ventilation after arrest, not
before

CONCLUSIONS
Beta-agonists

are first line therapy


Aminophylline does not have a role in the
management of acute asthma
Anticholinergics and magnesium may
improve PFTs in severe asthma
Consider using noninvasive ventilation
Intubation is based on clinical status, not on
numbers
Ventilator management is based on
permissive hypercapnea

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