Acute severe asthma (status asthmaticus)

• Status asthmaticus is a medical emergency, an extreme form of asthma exacerbation

characterized by hypoxemia, hypercarbia and secondary respiratory failure
• Status asthmaticus is an acute severe asthma attack that does not improve with usual doses
of inhaled bronchodilators and steroids. Signs and symptoms include hypoxemia, tachypnea,
tachycardia, accessory muscle use, and wheezing. Wheezing may be absent when airflow is
severely reduced. Rapid treatment is the key to preventing cardiopulmonary arrest. In
addition to usual and ongoing bronchodilators coupled with early steroids, other treatment
adjuncts exist.
• Etiology:
The time course of progression and the severity of airway obstruction follow two distinct
pattern
1. Slow onset asthma exacerbation
2. Sudden onset asthma exacerbation
 Factors that increase the risk of asthma related death

Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2018. Available from: www.ginasthma.org
Clinical features
ASSESSMENT Exacerbation severity
History: Physical Examination:
• Timing of onset and cause of the • Sign of exacerbation severity
present exacerbation • Complicating factors
• Sign of alternative condition (cardiac failure, inducible
• Severity of asthma symptoms laryngeal obstruction, inhaled foreign body or pulmonary
• Any symptoms of anaphylaxix embolism)
• Any risk factors for asthma
Objective measurement:
related death • Pulse oximetry  saturation levels <90%
• All current reliever and
• PEF (>5 years)
controller medications
Standard treatment
Adrenergic Agents
Adrenergic agents
• β-Adrenergic agonists with rapid onset are the preferred initial rescue medication for acute
bronchospasm
• Stimulation of β1-receptors increases rate and force of cardiac contraction and decreases small
intestine motility and tone, whereas β2-adrenergic stimulation promotes bronchodilation,
vasodilation, uterine relaxation, and skeletal muscle tremor.
• β-Adrenergic drugs cause bronchodilation by stimulation of the enzyme adenyl cyclase, which
converts intracellular adenosine triphosphate into cyclic adenosine monophosphate.
• β-Adrenergic drugs also inhibit mediator release and promote mucociliary clearance.
• The most common side effect of β-adrenergic drugs is skeletal muscle tremor, also may
experience nervousness, anxiety, insomnia, headache, hyperglycemia, palpitations, tachycardia,
and hypertension.
• Neither drug should be used for acute asthma exacerbations.
• Bronchodilator effects last at least 12 hours, and tachyphylaxis has not been reported with long-
term use.
Corticosteroid
• Corticosteroids are a cornerstone of asthma treatment.
• Steroids produce beneficial effects by restoring β-adrenergic
responsiveness and reducing inflammation.
• The peak anti-inflammatory effect occurs at least 4 to 8 hours after IV
or PO administration, but early use is wise to enhance care quickly;
corticosteroids given within 1 hour of arrival in the ED reduce the
need for hospitalization.
Anticholinergics
• The effects of anticholinergics used in combination with β-adrenergic agents are additive.
• Anticholinergics affect large, central airways, whereas β-adrenergic drugs dilate smaller
airways.
• Anticholinergic drugs competitively antagonize acetylcholine at the postganglionic junction
between the parasympathetic nerve terminal and effector cell.
• This process blocks the bronchoconstriction induced by vagal cholinergicmediated innervation
to the larger central airways.
• In addition, anticholinergics reduce concentrations of cyclic guanosine monophosphate in
airway smooth muscle, further promoting bronchodilation.
• The anticholinergic commonly used is inhaled ipratropium bromide.
• Potential side effects with anticholinergics include dry mouth, thirst, and difficulty swallowing.
Less commonly, tachycardia, restlessness, irritability, confusion, difficulty in micturition, ileus,
blurring of vision, or an increase in intraocular pressure can occur..
Magnesium
• IV magnesium sulfate is indicated in the management of acute, very
severe asthma (FEV1 <25% predicted
• When using magnesium in any form, monitor blood pressure and
deep tendon reflexes during administration because hypotension or
neuromuscular blockade may occur, although this is exceptionally rare
in the doses recommended.
Noninvasive positive-pressure ventilation
• Noninvasive positive-pressure ventilation improves airflow and
respirations compared with usual care, and despite little research, it is
commonly used in clinical practice for acute life-threatening asthma.
• Noninvasive positive-pressure ventilation decreases the need for
intubation, results in clinical improvement, and decreases the need
for hospitalization.
• Do not institute noninvasive positive-pressure ventilation if intubation
is indicated or in patients with suspected pneumothorax.
Ketamine
• Ketamine inhibits reuptake of noradrenaline and thus increases
circulating catecholamines, aiding some with severe asthma.
• If intubation is needed, ketamine is a good agent to aid during the
procedure and after mechanical ventilation starts.
Epinephrine
• Although epinephrine is standard treatment for anaphylactic asthma,
it is overlooked as an adjunct to treat status asthmaticus.
Mechanical ventilation
• If the patient manifests progressive hypercarbia or acidosis or becomes
exhausted or confused, intubation and mechanical ventilation are necessary to
prevent respiratory arrest.
• Mechanical ventilation does not relieve the airflow obstruction—it merely
eliminates the work of breathing and enables the patient to rest while the airflow
obstruction is resolved.
• The potential complications of mechanical ventilation in asthmatic patients
include extremely high peak airway pressures with subsequent barotrauma and
hemodynamic impairment.
• Mucous plugging is frequent, leading to increased airway resistance, atelectasis,
and pulmonary infection.
Agents of uncertain or no benefit in status
asthmaticus
• Heliox A mixture of 80% helium and 20% oxygen (heliox) can lower airway resistance and act as an adjunct in the
treatment of severe asthma exacerbations.43 Heliox does not reliably avert tracheal intubation, change intensive care
and hospital admission rates and duration, or decrease mortality in severe asthma.43
• Methylxanthines Aminophylline is no longer a first- or second-line treatment for acute asthma.44 The most common
side effects of methylxanthines are nervousness, nausea, vomiting, anorexia, and headache. At plasma levels >30
milligrams/mL, there is a risk of seizures and cardiac arrhythmias.
• Other Agents Mast cell modifiers, such as cromolyn and nedocromil, exert their anti-inflammatory action by blockage of
chlorine channels, modulating mast cell mediator release and eosinophil recruitment. These agents also inhibit early and
late responses to allergen challenge and exercise. Neither is indicated for treatment of acute bronchospasm.
• Leukotrienes are potent proinflammatory mediators that contract airway smooth muscle, increase microvascular
permeability, stimulate mucus secretion, decrease mucociliary clearance, and recruit eosinophils into the airway. Several
leukotriene modifiers, namely montelukast, zafirlukast, and zileuton, are available as oral tablets for the treatment of
asthma. Leukotriene modifiers improve lung function, diminish symptoms, and diminish the need for short-acting β2-
agonists. They may be used as an alternative to low-dose inhaled corticosteroid therapy in mild persistent asthmatics
and as steroidsparing agents with inhaled corticosteroids in moderate persistent asthmatics.7-10 Despite one trial with
adjuvant IV montelukast for acute asthma,45 there is no indication for the use of any of the leukotriene modifiers in the
ED.
Disposition and follow up
• Disposition decisions should take into account a combination of subjective parameters, such as resolution of wheezing and
improvement in air exchange, as assessed by auscultation and patient opinion; objective measures, such as normalization of FEV1 or
PEFR; and historical factors, such as compliance, history of ED use, and hospitalization. Some degree of residual airflow obstruction,
airway lability, and inflammation persists after treatment and discharge from the ED.
• Advise discharged patients to use a short-acting β-agonist on a scheduled basis for several days and to complete any oral
corticosteroids regimens. Add inhaled corticosteroids in patients with a history of persistent asthma who are not already using this
regimen.28-30
• A good response to treatment resolves symptoms and results in a PEFR or FEV1 of >70% predicted; these patients can be safely
discharged home. Patients with a poor response to treatment have persistent symptoms and FEV1 or PEFR of >70% predicted; these
patients can be safely discharged home. Patients with a poor response to treatment have persistent symptoms and FEV1 or PEFR of
<40% predicted; these patients are usually best observed or admitted. An incomplete response to treatment, the middle ground, is
defined as some persistence of symptoms and a PEF or FEV1 between 40% and 69% predicted. Most asthmatics treated in the ED fall
into this category and may be discharged home safely, although some benefit from prolonged observation or admission7-10 (Table 69-
2). Patients who fail to improve adequately over a period of several hours because they are in the late phase of their exacerbation and
those with significant risk factors for death from asthma are best placed in an observation unit or hospital bed. Many patients can be
successfully treated in an ED observation unit with evidence-based care protocols.46 Intubated patients require intensive care unit
admission. Arrange follow-up care to ensure resolution and to review the long-term medication plan for the chronic management of
asthma. High previous relapse rates suggest the need for follow-up within 1 to 4 weeks of the ED visit.7-10 Deliver an appropriate
written discharge plan of action that addresses routine care and care of worsening symptoms (Table 69-6).
Prognosis
• Poor Prognostic Factors
• If a complicating illness like congestive heart failure or chronic obstructive pulmonary
disease is not present, then status asthmaticus has a good prognosis provided treatment
has ensued timely. A delay in initiating the treatment is a bad prognostic factor.
• Adnet et al. evaluated complications and morbidities associated with a prolonged
neuromuscular blockade in status asthmaticus patients. The incidence of post-intubation
myopathy, ventilator-associated pneumonia, and duration of ICU stay were higher in the
neuromuscular blockade group in the population involving five centers.[11]
•  A study by Afessa et al. also reported a higher incidence of acidemia and carbon dioxide
retention in nonsurvivors than survivors with acute asthmatics.
• The need for mechanical ventilation has also been reported as a poor prognostic factor
Complications
• Acute hypotension on mechanical ventilation
• Other complication electrolyte abnormalities, hypotension and
dysrhythmias