by Krit kuruchaiyapanich R3

1. Acute Asthma in
Adults
Krit Kuruchaiyapanich, MD

2. Definition
 Asthma is a chronic inflammatory
disorder of the airways in which many
cells and cellular elements play a role.
◦ This inflammation causes recurrent
episodes of
wheezing, breathlessness, chest
tightness, and coughing, particularly at
night or in the early morning.
◦ Associated with widespread but variable
airflow obstruction that is often reversible
either spontaneously or withProgram, EPR3:
National Asthma Education and Prevention treatment.
Guidelines for the

3. Definition
 Status asthmaticus
◦ severe bronchospasm that does not
respond to aggressive therapies within 30
to 60 minutes.
 Near-fatal
◦ respiratory arrest or evidence of
respiratory failure (Paco2 > 50 mm Hg).

4. Definition
National Asthma Education and Prevention Program, EPR3:
Guidelines for the

5. Severe/Refractory asthma
American Thoracic Society workshop consensus for definition of severe/refractory
asthma (requires one or both major and two minor criteria and that other conditions
have been excluded, exacerbating factors have been treated, and patient is generally
compliant).

6. Pathophysiology
 Hallmark reduction in airway diameter
caused by
◦ smooth muscle contraction
◦ vascular congestion
◦ bronchial wall edema
◦ thick secretions
 Bronchoconstriction occurs due to
◦ 1. allergic  mediators and metabolic
products from inflammatory cells
◦ 2. nonallergic  exercise, aspirin-
induced, and menstrual-related asthma

7. Pathophysiology

8. Pathophysiology
National Asthma Education and Prevention Program, EPR3:
Guidelines for the

9. Pathophysiology
 Early asthmatic response
◦ Release of preformed histamine from
mast cell granules  bronchial smooth
muscle and airway edema wheezing
and airflow obstruction (resolves within an
hour )
 Late asthmatic response
◦ cytokines generated and released by
mast cells and other local and recruited
inflammatory cells prolonged airflow
obstruction and bronchospasm

10. Pathophysiology
 Eosinophils are major effector cells in
asthma
 Airway epithelial cells : produced Nitric
oxide (NO) potent vasodilator and may
reflect the presence of inflammation in
asthma
 Airway remodeling : Inflammation, mucus
hypersecretion , subepithelial fibrosis
airway smooth muscle
hypertrophy, angiogenesischronic
irreversible airflow limitation

12. Aspirin-exacerbated
respiratory disease (AERD)
 Triad
◦ aspirin sensitivity, asthma, and nasal polyps
 NSAIDs also precipitate AERD (but not
reported after administration of COX-2 inhibitors )
 common precipitant of life-threatening
asthma
 Symptoms
◦ occur within 3 hoursprofuse
rhinorrhea, conjunctival injection, periorbital
edema, and occasionally a scarlet flushing of
the head and neck
 Definitive diagnosis : provocation
challenges

13. Aspirin-exacerbated respiratory
disease (AERD)

14. Exercise-induced asthma (EIA)
 Etiology is unclear
 Atopy is strongly associated with
EIA, and up to 40% of patients with
allergic rhinitis have EIA
 Symptom
◦ occur 3-8 min of exercise, peak 8-15 min
after exercise, spontaneous recovery
occurs within 60 min
 Prophylaxis : warm-up and a short-
acting inhaled beta2-agonist

15. Menstruation-associated
asthma
 Perimenstrual reductions in PEFR of
35 to 80%
 Estradiol inhibits eosinophil
degranulation and suppresses LT
activity.
 Progesterone have bronchodilator and
anti-inflammatory activity.
 Tx : LT
antagonists, LABA , estradiol, progest
erone, and gonadotropin-releasing

16. CLINICAL FEATURES
 Classification
◦ 1. Type 1 (Slow onset> 6 hr) 80-90%
 Female>male
 Etiology: URI
 Inflammation less severity than type 2
 slower response to therapy
◦ 2. Type 2 (Sudden onset< 6 hr) 10-20%
 Male>female
 Etiology: respiratory allergen, exercise, stress
 Bronchoconstriction more severe
 faster response to therapy
Picado C. Classification of severe asthma exacerbations: a proposal. Eur Respir J

17. CLINICAL FEATURES
 Symptom : Triad
◦ dyspnea, wheezing, and cough
 Early chest constriction and cough
 Exacerbation progresses
wheezing, prolonged expiration and
accessory muscle used(indicates
diaphragmatic fatigue)
 Tachypnea and tachycardia >120
beats/min are associated with severe
obstruction, but a lower rate does not
R/O severe asthma.
 The "silent chest" reflects very severe

18. CLINICAL FEATURES
 bronchiolar smooth muscle tone
airway resistance, pulponary
infiltration, V/Q missmatch
 Dynamic hyperinflation auto-PEEP
pulsus paradoxus, diastolic LV dysfn
 Acute hypercapnia+ intrathoracic
pressure ICP
 Signs of impending respiratory failure (1)
◦ inability to speak, altered mental
status, intercostal retraction, worsening
fatigue, and a PCO2 of ≥42 mmHg
(1) National Asthma Education and Prevention Program, EPR3:
Guidelines for the

19. SEVERITY OF ASTHMA
EXACERBATIONS
National Asthma Education and Prevention Program, EPR3:
Guidelines for the

20. Risk factors for death from
asthma

23. DIAGNOSTIC STRATEGIES
 Pulmonary Function Studies
◦ FEV1 or PEFR
◦ the best of 3 consecutive values should be
recorded
 Arterial Blood Gas (mild to moderate hypoxemia
with resp. alkalosis)
◦ 1. predicted PFTs of < 30%
◦ 2. clinical course is perplexing Indication
◦ 3. capnography is not available.
◦ acute ventilatory failure hypoventilation
with CO2 retention and resp. acidosis

24. DIAGNOSTIC STRATEGIES
 CXR suspected…
◦ pneumonia, pneumothorax, ateltctasis, pn
eumomediastinum, or CHF
 ECG should not be routinely
obtained, except
◦ patients >40 yr, a separate complaint
(e.g., chest pain), Hx of significant CVD
◦ severe asthma: a RV strain pattern
 Others
◦ LTE4 in the urine
◦ exhaled nitric oxide

25. Assessment Summary
 The severity of airflow obstruction
cannot be accurately judged by
patients’ symptoms, PE , and
laboratory tests. Serial measurements
of airflow obstruction (FEV1 or PEFR)
are key components of disease
assessment and response to therapy .

26. Peak Flow Meter

27. Management
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

28. Management
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

29. Management
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

30. Management
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

33. Medication
The goal of treatment of acute asthma in
the ED is to reverse airflow obstruction
rapidly by repetitive or continuous
administration of inhaled B 2-
agonists, ensure adequate oxygenation, and
relieve inflammation

34. Medication
1. Relievers
- B2-
adrenergic , Anticholinergics, Theophyli
ne
2. Controller
- Glucocorticoids, Leukotriene
modifiers, Cromones, Anti-IgE

35. β2-Adrenergic Agonists
 Relaxation of bronchial smooth
muscle, inhibit mediator release and
promote mucociliary clearance.
 Most common side effect: skeletal
muscle tremor.
◦ others:
nervousness, anxiety, insom
nia, headache,
hyperglycemia, palpitations,
tachycardia, and hypertension.

36. β2-Adrenergic Agonists
 SABA (Solution=MDI)
◦ First line drug
◦ Nebulization = MDI + spacer (prefer
nebulization)
◦ Salbutamol 2.5 – 5 * 3 time/hr
◦ MDI with spacer 4– 8 puffs q 20 min up to
4 h, then q 1–4 h as needed.

37. β2-Adrenergic Agonists
 IV form (not recommened in USA)
◦ severe nonresponsive acute asthma.
◦ albuterol loading dose 4 μg/kg for 2-5 min
then infusion of 0.1 to 0.2 μg/kg/min
◦ Epinephrine IV titrated to effect (average 1.5
μg/min with a range of 0.5–13.3 μg/min)
 SC form
◦ may be used in pt who cannot adequately
inhale albuterol or who experience severe
bronchospasm.
◦ Epinephrine (1:1000 ) 0.2-0.5 mL q 20 -30
min
◦ Terbutaline 0.25 mg SC q 20 min * 3 dose

38. Corticosteroids
 Action in the airways
◦ inhibition of recruitment of inflammatory cells
and inhibition of release of proinflammatory
mediators and cytokines from activated
inflammatory and epithelial cells, activate
cytoplasmic glucocorticoid receptors to
regulate directly or indirectly the transcription
of certain target genes resulting in the
synthesis of new proteins.
 Two forms
◦ 1. Systemic
◦ 2. Inhaled

39. Corticosteroids
 1. Systemic (IV and oral)
◦ speeds the resolution of airflow
obstruction, reduces the rate of relapse and
may decrease admissions in severe, but
not in mild to moderate attacks.
◦ Prednisone 40-60 mg oral loading
◦ Methylprednisolone 40–80 mg/day in one
dose or two divided doses
◦ Demethasone 5 mg
◦ given q 6 hr until PEFR reaches 70% of
predicted value or a personal best value

40. Corticosteroids
 IV = oral
 Side effects
◦ short-term (hours or days) reversible
increases in glucose (important in
diabetics) and decreases in
potassium, fluid retention with wt
gain, mood alterations including rare
psychosis, hypertension, peptic
ulcers, aseptic necrosis of the femur

41. Corticosteroids
 2. Inhaled
 ICS + SABA NB: reducing airway reactivity and
edema more effectively
 reduce rates of hospitalization
 Side effect : Dysphonia, Reflex cough and
bronchospasm, Oral candidiasis
 Discharged
 Prednisone 40-60 mg oral for 7 day
 ICS high-dose budesonide (400 μg, two puffs
twice per day)

42. Anticholinergic Agents
Atropa Belladonna
Leave

43. Anticholinergic Agents
 Block smooth muscle constrictor and
secretory consequences of the
PNS, blocking reflex bronchoconstriction
and reversing acute airway obstruction.
 affect large, central airways, but
adrenergic drugs dilate smaller airways.
 Side effect
◦ dry mouth, thirst, and difficulty swallowing. Less
commonly, tachycardia, restlessness, irritability,
confusion, difficulty in micturition, ileus, blurring
of vision, or an increase in IOP

44. Anticholinergic Agents
 Inhaled-ipratropium bromide
◦ Nebulizer solution (0.25 mg/ml) 0.5 mg q 20
min for 1 hr (three doses), then as needed;
◦ MDI (18 μg/puff) 8 puffs q 20 min as
needed, for up to 3 hr
◦ not recommended as monotherapy in ED
slow onset of action
◦ added to SABA for a greater and longer-
lasting bronchodilator effect, reduce rates of
hospitalization by approximately 25% in
severe asthma
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

45. Magnesium Sulfate
 relaxes bronchial smooth muscle and
dilates asthmatic airways.
 I/C (recommended IV > NB)
◦ severe asthma attacks (FEV1 < 25%
predicted) improves airflow obstruction and
decreases the need for hospital admission
◦ MgSO4 2 -3 g IV over 20 min or at rates of
up to 1 g/min to patients with severe
refractory asthma
 Side effect
◦ warmth, flushing, sweating, N/V, muscle
weakness and loss of DTR, hypotension, and
respiratory depression.

46. Treatments That Are Not
Recommended
 1. Methylxanthines
◦ lack of demonstrated efficacy and increases
in adverse events
 2. Antibiotics
◦ should be reserved for pt with bacterial
infection (e.g., pneumonia or sinusitis)
seems likely.
 3. Aggressive hydration
 4. Mucolytic agents
◦ worsen cough or airflow obstruction
 5. Sedation
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

47. Leukotriene Modifiers
 non-beta-mediated bronchodilating
effects
 Zafirlukast (20 mg twice a day)
 Montelukast (10 mg daily)
 Currently, there is no indication for the

48. Pregnancy
 The principles of managing acute asthma in
pregnancy and during lactation are similar
to those for the nonpregnant state.
 Early intervention during acute
exacerbation is key to the prevention of
impaired maternal and fetal oxygenation.
 PaO2 <70 mm Hg  severe hypoxemia
 PaCO2 >35 mm Hg  respiratory failure
 B2-agonist and ICS : safe during pregnancy
and are recommended as a routine part of
asthma management

49. NPPV
 BiPAP
◦ well tolerated by children , decrease the
need for intubation and mechanical
ventilation.
◦ Consider for pt. who decline intubation
and pt. who cooperate with mask therapy
◦ but more data are needed to recommend
this approach
 Patient must be alert mental status
and intact airway reflexes
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

50. Ketamine
 potent bronchodilator effects
 no randomized trials have been
conducted.
 not recommended for therapy of acute
asthma in the nonintubated patient
 Ketamine 1–2 mg/kg IV
 Side effect
◦ increased airway secretions and
emergence reactions

51. Intubation and Ventilator
Strategy
 Avoid nasotracheal route
 Intubate before the crisis of respiratory
arrest
 Selected largest ET-tube as soon as
possible.
 Pretreatment
◦ Lidocaine 1.5 mg/kg IV
 Induction
◦ Midazolam 1 mg IV q 2-3 min
◦ Ketamine 1–2 mg/kg IV
 Neuromuscular blocking agent
◦ Preferred Rocuronium (1 mg/kg) >
Rodrigo GJ, Rodrigo C, Hall JB. Acute asthma in adult: a review. Chest 2004; 125:

52. Intubation and Ventilator
Strategy
 Ventilator strategy
◦ adequate oxygenation and
ventilation, minimizing high airway
pressure, barotrauma, and systemic
hypotension
 Permissive hypercapnia technique
◦ TV 6–8 mL/kg, MV 6-8 LPM
◦ I:E > 1:3, RR 11-14 /min
◦ End-inspiratory pressure < 35 cmH2O
◦ pH maintained at 7.15–7.2
◦ Paco2 <100 mm Hg

53. Intubation and Ventilator
Strategy
 Complications of mechanical
ventilation
◦ Hypotension and barotrauma
◦ Pneumothorax !!!
 sudden clinical deterioration
 hypotension
 significant rise in peak inspiratory ventilator
pressures and falling oxygen saturation.
 External lateral chest compression :
patients cannot exhale esp; children

54. Cardiopulmonary arrest
 May result from unrecognized
barotrauma.
◦ Empirical bilateral tube thoracostomy
should be performed if unexplained
cardiac arrest occurs, especially in the
context of dramatic increases in peak
inspiratory pressure.
◦ IV epinephrine has both cardiostimulatory
and bronchodilatory properties.

55. DISPOSITION
 When should be discharged
◦ FEV or PEF after treatment is >= of the
11
personal best or predicted value
◦ Improvements in lung function and
symptoms > 60 min
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

56. DISPOSITION
Emergency Treatment of Asthma, N ENGL J MED 363;8 nejm.org august

58. THANK YOU