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Status Asthmaticus

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Title: Status Asthmaticus


1
Status Asthmaticus
  • Jack L-M Mutnick, MD
  • University of Minnesota
  • PGY-3

2
Terminology
  • Severe attack of asthma poorly responsive to
    adrenergic agents and associated with signs or
    symptoms of potential respiratory failure

3
Etiology
  • The disease (of asthma) has its roots in infancy
  • Causes include
  • Genetic (atopy IgE mediated allergic response)
  • Environmental Factors
  • Viruses
  • Allergens
  • Occupational Exposures

4
Pathogenesis
  • Pathologic changes on Post-mortem of airways
    shows
  • Bronchial wall thickening 2/2 edema, inflammatory
    cell infiltration
  • Hypertrophy hyperplasia of Bronchial smooth
    muscle, submucosal glands
  • Collagen deposition beneath basement membrane
  • In addition, many deaths are associated with
  • Intraluminal inspissation of secretions (mucus
    plugging)
  • If mucus is absent, suggests airway obstruction
    was due to intense smooth muscle contraction

5
Clinical Danger Signs
  • Use of accessory muscles of respiration
  • Brief, fragmented speech
  • Inability to lie supine
  • Profound diaphoresis
  • Agitation
  • Severe symptoms that fail to improve with initial
    emergency department treatment
  • Life-threatening airway obstruction can STILL
    OCCUR when these signs are not present

6
Dont Even Wait If.
  • Inability to
  • 1. Maintain respiratory effort
  • 2. Cyanosis
  • 3. Depressed mental status
  • All three foreshadow imminent respiratory arrest
  • DONT WAIT ? INTUBATE

7
Diagnosis
  • Hx most powerful predictor that this may be
    life-threatening is a prior intubation for an
    asthma attack
  • PEX alteration in consciousness, fatigue,
    upright posture, diaphoresis, accessory muscle
    breathing.
  • Tachycardia, tachypnea, pulsus paradoxus
  • IMPORTANT look in the mouth as obstruction might
    be in the upper airway (epiglottitis, angioedema)
  • Peak Flow (PEFR) if pt is not too dyspneic. Best
    measure of severity

8
Diagnosis
  • ABG Look at PaCO2. Resp drive almost always
    increased in acute asthma ? hyperventilation ?
    decreased PaCO2.
  • Thus, an elevated or normal PaCO2 indicates
    airway narrowing is so severe that the
    ventilatory demands cannot be met. Failure is
    imminent
  • CXR usually not helpful
  • Obtain if diagnosis is in doubt, patient is
    high-risk (IVDU, immunosuppressed, chronic
    pulmonary disease), or if complications are
    suspected (pneumothorax)

9
Acute Management
  • Oxygen
  • severe hypoxemia is unusual in acute asthma but
    low flow supplemental O2 carries almost no risk
    (maintain SaO2gt92)
  • Inhaled Beta Agonist
  • Albuterol Neb continuously or 2.5mg Neb q15
  • Initial goal is to reverse obstruction
    emergently, with the ultimate goal to be
    sustained improvement
  • Monitor electrolytes (e.g.... Potassium)
  • IV Access
  • May want to give a bolus of NS for prolonged
    episode to replace insensible losses

10
Acute Management
  • Parenteral Magnesium
  • 2 grams over 20 minutes
  • Bronchodilator activity, inhibits calcium influx
    into smooth muscle
  • Corticosteroids
  • Methylprednisolone 60-125mg IV or Dexamethasone
    6-10mg IV or prednisone 40-60mg po
  • Early administration dramatically reduces
    hospitalization and the likelihood of death from
    acute asthma
  • Much improves FEV1 at 24 hours
  • The slowness of its response DOES NOT diminish
    its importance

11
Additional Treatments
  • Terbutaline ? 0.25mg SC q20 x 3 doses
  • For severe asthma unresponsive to standard
    therapies give terbutaline OR epinephrine but
    NOT both
  • Epinephrine ? 0.2-0.5mL of 11000 by SC injection
  • For severe asthma unresponsive to standard
    therapies once again, give terbutaline OR
    epinephrine but NOT both
  • Heliox (helium and oxygen)
  • May improve ventilation and decrease work of
    breathing with acute, severe airflow obstruction.
  • Be careful not to lower pts oxygen saturation
    controversial treatment

12
Intubation
  • Decision to intubate in the first few minutes is
    CLINICAL
  • In the absence of anticipated intubation
    difficulty, rapid sequence intubation is
    preferred.
  • Nasal intubation is not recommended
  • Goal is to maintain adequate oxygenation and
    ventilation while minimizing elevated airway
    pressures therefore,
  • High Inspiratory flow rates (80-100L/min), low
    tidal volumes (6-8mL/kg), and low respiratory
    rates (10-14/min)
  • In some patients, permissive hypercapnia is
    acceptable to avoid barotrauma

13
Controversial
  • It is not established whether ipratropium by
    inhalation, or theophylline by IV, adds to the
    bronchodilation achieved by maximal doses of
    inhaled beta agonist alone.
  • Ipratropium bromide some studies state addition
    of 0.25mg ipratropium to albuterol neb might
    confer some additive benefit over albuterol alone
  • Theophylline IV Contradictory results
  • Some studies show it adds toxicity but has no
    influence on the course or duration of
    hospitalization, or immediate bronchodilation
  • Positive results are few and far between
  • The weight of evidence shows little or no
    significant benefit for acute bronchodilation,
    and has significant toxicity
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