Asthma in ED

1. ASTHMA
Dr. Agh Pakniyat

2. EPIDEMIOLOGY
• children than adults, in females than males, and in blacks than whites or
Hispanics.
• more prevalent in the impoverished and in those residing in
nonmetropolitan locales.
• Factors that contribute to asthma morbidity and mortality :
 inadequate patient and physician assessment of an acute episode
resulting in under treatment
 overuse of prescribed or over-the-counter medications leading to delays in
seeking treatment
 failure of physicians to consider previous ED visits,hospitalizations, or life-threatening
episodes of asthma
 failure to initiate corticosteroid therapy early in the course of an
exacerbation.
 Socioeconomic factors, environmental influences, and overreliance on
emergency facilities for all asthma care are also contributing factors.

3. PATHOPHYSIOLOGY
• Increased expiratory resistance:
 Airway inflammation
 Bronchospasm
 Mucosal edema
 Mucous plugging
 Smooth muscle hypertrophy
• Consequences:
 Air trapping
 Airway remodeling
 Increased dead space
 Hyperinflation

5.  Pollen
Dust mites
Molds
 Animal dander
Other environmental
allergens
 Viral upper
respiratory infections
Occupational
chemicals
 Tobacco smoke
 Environmental
change
Cold air
 Exercise induced
 Emotional factors
Menstrual associated
Drugs:
Aspirin
NSAIDs
β-blockers
Triggers:

6. • Mast cell stabilizers (e.g., beta-agonists) are
more effective in the early asthmatic
response but are of less use later in the
course of an exacerbation. Anti-inflmmatory
therapy (e.g., corticosteroids, LT antagonists)
is more effective in the late asthmatic
response.

9. ASPIRIN-EXACERBATED RESPIRATORY DISEASE
(AERD) :
 nasal polyps
 eosinophilic sinusitis
 asthma
 and sensitivity to cyclooxygenase (COX)-1
inhibitor drugs (e.g., aspirin)
adult>pedi
Femal>male
average age of onset is 34 years, frequently
after a
viral respiratory illness.

10. • acute asthma symptoms occur within 3 hours,
• accompanied by profuse rhinorrhea,
conjunctival injection, periorbital edema, and
occasionally a scarlet flshing of the head and
neck

12. AERD RX :
o block synthesis of LTs (e.g.,
zileuton)
o block specifi LT receptors (e.g.,
zafilukast, montelukast).

13. • AERD is not reported after
administration of COX-2 inhibitors.
Most patients with AERD can tolerate
up to 500 mg of acetaminophen safely,
but 28 to 34% experience mild
respiratory reactions when
administered 1000 to 1500 mg.
Reactions to acetaminophen tend to be
milder than those to NSAIDs.

14. EXERCISE-INDUCED ASTHMA (EIA):
 Prophylaxis :short-acting inhaled
beta-agonist
 Pretreatment with cromolyn, LT antagonists
(montelukast), and inhaled parasympatholytics is
also effective.
 Breathing through the nose may allow warming
and humidification of cool dry air during
exercise.
Long-acting beta-agonists are usually
effective, but tachyphylaxis and loss of efficacy
may occur if these agents are used regularly

15. MENSTRUATION-ASSOCIATED ASTHMA
• Perimenstrual reductions in peak expiratory
flew rates (PEFRs) of 35 to 80% are reported.
• Estradiol inhibits eosinophil degranulation
and suppresses LT activity.
• Progesterone may also have bronchodilator
and antiinflmmatory activity, and the rapid
decline in progesterone levels before
menstruation may contribute to increased
bronchospasm.
• Rx: LT antagonists, long-acting beta-agonists,
and oral contraceptives.

17. DIAGNOSTIC STRATEGIES
• PFT
• Therefore routine PFT should be part of ED
assessment and monitoring.
• The forced expiratory volume in 1 second from
maximal inspiration (FEV1) or the PEFR in liters
per second, starting with fully inflted lungs and
sustained for at least 10 msec, may be used.
• Any patient not able to perform a pulmonary
function study should be considered to have
severe airway obstruction.

18. ABG;
 hyperventilation leads to a modest fall in the
partial pressure of carbon dioxide in arterial
blood (Paco2). As airway obstruction increases,
the Paco2 normalizes (PFT values 15-25%
predicted) and then increases (PFT values <15%
predicted) with worsening hypoxemia.
 ABG determination is rarely clinically useful
in acute asthma exacerbations unless oxygen
saturation cannot be obtained reliably via
pulseoximetry.
 ABG sampling should be limited to a subset of patients
with predicted PFT values of less than 30%, whose
clinical course is perplexing, and for whom capnography
is not available.

19. • Laboratory studies rarely are helpful in
evaluating the patient with an acute
asthma attack.
• Leukocytosis
• In the older asthmatic with cardiovascular
comorbidities, measurement of the B-type
natriuretic peptide (BNP) level may reveal
unrecognized congestive heart failure.
• Serum electrolytes are not primarily
altered unless the patient is taking
corticosteroids or diuretics or has
cardiovascular disease and is receiving
aggressive beta2-agonist therapy.

20. CXR :
 complicating cardiopulmonary process,
such as pneumonia, pneumothorax,
pneumomediastinum, or congestive
heart failure.
 patients who do not respond to
optimal therapy and require
hospital admision.
 First presentation

21. ECG :
• If :chest pain or a history of significant cardiovascular disease, in whom the
asthma attack may be a physiologic stress test.
 continuous cardiac monitoring :
 Older patients, especially those with coexistent heart disease or with severe
exacerbation
 severe hypoxemia
 intubation is contemplated.
o Transient changes in severe asthma:
 Right axis deviation
 Right bundle branch block
 Abnormal P-waves
 Nonspecific ST–T-wave changes:severe right ventricular strain pattern
that reverses with improvement in airflw.

22. • cytokine profies in the blood
• evaluation of LTE4 in the
urine
• monitoring of exhaled
pentane, hydrogen peroxide,
NO, or carbon monoxide
levels
exhaled NO, a marker of
airway inflmmation.

24. MANAGEMENT OF ACUTE EXACERBATION:
PRE HOSPITAL :
• Recognize the “quiet chest” as respiratory
distress.
• increased use of inhaled beta2-
agonists
• early administration of
systemic corticosteroids (not
simply doubling the dose of
current ICSs)

25. MANAGEMENT OF ACUTE ASTHMA IN
THE EMERGENCY DEPARTMENT
•Oxygen
Administration:
Goal : arterial oxygen saturation above 90%
(above 95% in pregnant women and those with
coexistent heart disease).
Humidification of the inspired air oxygen
mixture is not essential.

26. ADRENERGIC MEDICATION:
•Guidelines for chronic
use of inhaled beta2-
agonists,, recommend
limited daily use in a
rescue-only mode.

27. SHORT-ACTING INHALED BETA2-AGONIST
CHOICE AND ADMINISTRATION SCHEDULE.
• more beta2-selective
 In chronic asthma, levalbuterol provides a better
therapeutic index
 An MDI plus a valved holding chamber (“spacer”)
provides similar bronchodilation and side effects,
even in severe asthma, when compared with wet
nebulization.
 Epinephrine is used cautiously in patients older than
40 years or those with suspected cardiovascular
disease, (average 1.5 μg/min with a range of 0.5-13.3
μg/min)
 The PFT response to the initial bronchodilator
therapy over the initial 15 to 60 minutes is a better
predictor of the need for hospitalization than is the
severity of an exacerbation.
 Subcutaneous adrenergic agents = aerosol delivery.
(1 : 1000 solution 0.2 to 0.5 mL q 20 to 30 minutes up to
3 dose).

28. LONG-ACTING BETA2-AGONISTS
(LABAS) AND ACUTE DISEASE.
• It has an onset of action of 20 minutes
and thus is not a rescue medication.
• contraindicate chronic
use in patients of all ages
without concomitant use
of an asthma controller
medication such as an
ICS

29. SYSTEMIC CORTICOSTEROIDS IN THE EMERGENCY
DEPARTMENT
 moderate to severe attacks
 experiencing an incomplete response to initial beta-agonist
therapy
 taking oral corticosteroids or ICSs
• Oral 60 mg
• Im 40-80 mg
• may decrease admissions only in severe mode
• Continuing therapy with oral prednisone or prednisolone is given in
an adult dose of 40 to 80 mg/day, usually as a single dose.

30.  Side effects :
1. reversible increases in glucose (important in diabetics)
2. decreases in potassium
3. fluid retention with weight gain
4. mood alterations including rare psychosis,
5. Hypertension
6. peptic ulcers,
7. aseptic necrosis of the femur
8. and rare allergic reactions.
 Evidence suggests that treating both systemically and via airway with
corticosteroids in acute disease is more effective than either treatment
method alone.
 An acceptable regimen is 40 to 60 mg of prednisone (or equivalent) in
single daily dose for a total of 5 to 10 days. Dose tapering for patient was
already receiving systemic steroid.
• An alternative approach, if compliance or inability to obtain oral corticosteroids
is an issue, is to give an equally efficacious single depot dose of
dexamethasone 10 mg, triamcinolone diacetate 40 mg, or
methylprednisolone 160 mg before ED discharge.
 addition of inhaled high-dose budesonide (400 μg, two puffs twice per
day)

31. • The maximum effect with inhaled ipratropium is in 30 to 120
minutes, with the effect lasting up to 6 hours. it should not be used
alone for therapy of acute asthma attacks.
 Ipratropium may be more effective in :
• patients older than 40 years,
• bronchospasm secondary to beta blocking agents
• psychological factors contribute to their disease.
 Magnesium adjunctive administration in severe asthma attacks
(FEV1 <25% predicted) improves airflow obstruction and
decreases the need for hospital admission
 administer 2 to 3 g of intravenous magnesium sulfate over 20
minutes or at rates of up to 1 g/min to patients with severe
refractory asthma while continuing aggressive inhalation
therapy.
• Side effects :warmth, flushing, sweating, nausea and emesis,
muscle weakness and loss of deep tendon reflexes, hypotension,
and respiratory depression.

32. • Methylxanthines:
• Not recommended in acute asthma.
• Leukotriene Modifirs:
 Zafilukast (20 mg twice a day) and montelukast (10 mg
daily) are rapid-acting, safe, oral asthma controller drugs
that are potent and highly selective antagonists of type 1
cysteinyl LT receptors.
 Consider Antibiotic

34. PREGNANCY AND ACUTE ASTHMA:
• The effect of pregnancy on asthma is unpredictable.
• severity = risk of severe exacerbation.
• Obesity and female fetal sex =increased risk of
exacerbation.
• severe asthma =gestational diabetes and delivery before
37 weeks.
• The hyperventilation of pregnancy is compensated for by
a metabolic acidosis. Typical pregnant patients have
ABGs with a pH of 7.40 to 7.45, Po2 of 106 to 110, and
Pco2 of 28 to 32 mm Hg;
therefore when ABG values in a pregnant patient are
interpreted, a normal Pco2 actually represents
hypercarbia. Maternal hypoxemia quickly results in fetal
hypoxemia. PEFR remains unchanged during
pregnancy, and monitoring in the ED is
strongly recommended.

35. SEVERE, NEAR-FATAL, AND FATAL ASTHMA
•

36.  Clinical features of severe asthma ;
• lesser prevalence of atopy
• a history of aspirin sensitivity
• higher incidence of sinusitis
• use of nasal corticosteroids (suggesting involvement of the upper as well as
the lower respiratory tract).
• associated with menses.
 Status asthmatics : severe bronchospasm that does not respond to
aggressive therapies within 30 to 60 minutes.
 Near fatal asthma :respiratory arrest or evidence of respiratory failure (Paco2
above 50 mm Hg).
o Slow-onset near fatal asthma: several days
o Rapid-onset near-fatal asthma: 3 hrs
 It is interesting to note that the hypercapnia in rapid-onset
near-fatal asthma is more responsive to therapy
than that in the slow-onset type, and these patients
require shorter durations of mechanical ventilation

37. CLINICAL APPROACH TO THE CRITICALLY ILL
ASTHMATIC
Alterations in consciousness
and bradypnea indicate
hypercarbia and impending
respiratory arrest.
• Persistent elevations of arterial lactate levels are
often associated with a poor prognosis. An elevated
lactic acid level is not predictive of respiratory failure
in critically ill asthmatics, and blood lactate levels are
not generally prognostic.

38. NONINVASIVE STRATEGIES.
 continuously nebulized beta and anticholinergic agents
 If parenteral adrenergic therapy is desired, terbutaline is preferred
because of its beta2 selectivity.
 Intravenous magnesium sulfate or beta-agonists (where available)
may be of benefi.
 Oral prednisone 60 mg or intravenous methylprednisolone 125 mg
 Helium:
 Mixture of helium and oxygen (80:20, 70:30, 60:40)
Less dense than air
Decrease airway resistance.
Decrease in respiratory exhaustion
Not currently recommended for routine use

Noninvasive positive-pressure ventilation may benefit carefully selected
patients
 May improve oxygenation and decrease respiratory fatigue
 Can only be used in an alert patient
 Should not replace intubation
Not currently recommended for routine use

39. INTUBATION AND VENTILATOR
STRATEGY
• Indications for intubation in the asthmatic patient :
• coma, altered consciousness, cardiac or respiratory arrest, paradoxical
breathing pattern, refractory hypoxemia, and failure of NIPPV.
• threshold levels for intubation based on ABG results, but there is no evidence
that ABG results provide better guidance regarding need for intubation than
does overall clinical assessment.
• Rapid sequence intubation
Lidocaine to attenuate airway reflexes
Etomidate or ketamine as an induction agent
Succinylcholine should be administered to achieve paralysis.
A large endotracheal tube > 7 mm should be used to facilitate ventilation.
May need to mechanically exhale for the patient
Permissive hypercapnia

40. • Ketamine (1-2 mg/kg) is the preferred
agent for induction in rapid sequence
intubation of the asthmatic patient.
•
Bronchodilator and an anesthetic agent
Useful as an induction agent during
intubation
•
Contraindications:
HTN
Coronary disease
Preeclampsia
Increased intracranial pressure

41. ADMISSION CRITERIA
MEDICAL WARDS
• PEFR < 40% and minimal air movement
Persistent respiratory distress:
 Factors that should favor admission:
 Prior intubation
 Recent ED visit
 Multiple ED visits or hospitalizations
 Symptoms for more than 1 wk
 Failure of outpatient therapy
 Use of steroids
 Inadequate follow-up mechanisms
 Psychiatric illness

42.  Observation Unit
 PEFR > 40% but < 70% of predicted
 Patients without subjective improvement
 Patients with continued wheeze and diminished air movement
 Patients with moderate response to therapy and no respiratory distress
 Discharge Criteria
PEFR > 70% should be > 300
Patient reports subjective improvement
Clear lungs with good air movement
Adequate follow-up within 48–72 hr

43. PEARLS AND PITFALLS
Altered mental status in asthma equals ventilator
failure.
Patients should be able to demonstrate the
correct use of their inhaler or
nebulizer:Discharge with a peak flow meter
 If no signs or symptoms of dehydration, no
evidence that IVF will clear airway secretions.
Antibiotics should generally be reserved for
patients with purulent sputum, fever, pneumonia,
or evidence of bacterial sinusitis.