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

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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

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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