Management of Severe Asthma Exacerbation and Recognition
of Acute Respiratory Failure by Dr. Roubing Wang and Dr. Kenan
Haver.
Today I'll be talking about asthma exacerbation inpatient
treatment.
The case is that of a 13-year-old boy
with severe persistent asthma who
is maintained on high dose inhaled corticosteroid
plus a long-acting beta-agonist who
was admitted to the pulmonary service for asthma
exacerbation.
He has a history of multiple admissions,
including one ICU admission, but no intubations.
He received several courses of oral steroids in a whole year.
Prior to admission, he developed increased shortness of breath
and coughing in the setting of an upper respiratory infection.
In the emergency room his lung exam
was consistent with expiratory wheezing and decreased
aeration.
He was diagnosed with an asthma exacerbation.
He received stacked beta-2 agonist and oral steroids
in the emergency room.
And while inpatient, he was receiving beta-2 agonist
every two hours.
The nurse pages you at this time as the patient
is complaining of chest tightness
after one hour albuterol.
And he seems to be in distress.
The biggest challenge in asthma exacerbation
is identifying the patient at risk for deterioration.
Initiation of timely and appropriate treatment
may prevent an adverse or even fatal outcome.
The questions to ask on the phone are,
what are the current vitals?
And that includes respiratory rate, oxygen saturation,
heart rate, and blood pressure.
If not yet done, obtain the vitals
and place a patient on a cardiopulmonary monitor.
Go assess the patient immediately.
When you're in the room, ensure the patient's connected
to a cardiopulmonary monitor.
Ensure the presence of adequate personnel in the room.
And ensure action to the resources nearby.
Do not forget your ABCs.
Assess the airway.
Is the patient speaking or crying?
Assess breathing.
How is the respiration rate and oxygen saturation level?
How is the circulation?
Assess the heart rate and perfusion.
For physical exam, concentrate first
on the general distress level.
Is there accessory muscle use?
Is the patient able to speak in full sentences?
How is the mental status and the level of consciousness?
How is the coloring of the patient?
Is the patient cyanotic or pale?
Chest exam.
Focus on increased work of breathing.
Again focus on accessory muscle use, retractions
in younger patients, and nasal flaring in infants.
Auscultation of the chest.
Please focus on wheezing, inspiratory
to expiratory ratio, and air movement.
Patient in classic asthma exacerbation
usually will have diffused polyphonic expiratory wheezing,
increased expiratory phase, and diminished air movement.
These findings may vary based on the limitation of airflow.
The presence of silent chest can be
a dire sign of imminent cardiopulmonary failure.
Also assess the presence of focal exam,
such as absence of breath sounds on one
side or the presence of focal crackles, which may indicate
pneumothorax or pneumonia.
For the cardiac exam, assess the heart rate,
which may be increased due to bronchodilators use.
The presence of bradycardia can be a sign
of life-threatening disease.
Assess for the presence of pulsus paradoxus, which
is a decrease in systolic blood pressure
of greater than 10 millimeters of mercury
during inspiration, which can be a sign of severe exacerbation.
Point of clarification.
Determining the presence of pulsus paradoxus
may be difficult without an arterial line.
However, you may have a suspicion
for it based upon feeling a change in the pulse strength
during pulpation and/or by seeing
a variation in the amplitude on the pleth tracing
on your saturation probe.
Presence of rash or hives may alert the physician
to the diagnosis of anaphylaxis.
A brief history may be attained while the patient's
being examined.
The priority is to identify quickly the patient at risk
for adverse or fatal outcomes.
Questions may include, when was the last dose of bronchodilator
administered?
Was there any instigating events, such as exposure
to allergens or irritants, food, new fevers, rhinorrhea,
or ill contacts?
Remove possible offending agent if present.
If the ingestion of food precedes the attack,
one may consider the presence of anaphylaxis.
Ask the patient for symptoms such as chest tightness,
dyspnea, chest pain, dizziness, palpitations,
or throat tightness.
The presence of throat tightness may
indicate a possible concurrent vocal cord impairment.
Identify risk factors for death from asthma,
such as asking about previous asthma attacks
with respiratory failure, seizures,
loss of consciousness, intubations, and ICU stays.
The presence of poorly controlled asthma
prior to admissions by asking the frequent beta-agonist use,
recent hospital admissions, or the use of many maintenance
medications to achieve control.
Ask about poor self-perception of symptoms,
such as a disease severity and the inability
to sense critical or worsening bronchospasm.
Ask about the history of underutilization
of medical resources, non-compliance, psychosocial
economic problems.
Labs and chest X-rays are usually not
necessary an emergent situation but
may be helpful to identify alternative or concurrent
diagnosis and/or monitor side effects of current medications.
Labs such as an arterial blood gas or a venous blood gas
may be considered to help guide severity
and need for intubation.
A chem-10 may be checked as therapies may
lead to electrolyte imbalance.
For example, albuterol can lead to hypophosphatemia
or hypokalemia.
Unless an alternative diagnosis, such as infections, is raised,
labs such as a CBC or blood cultures
are not necessary and routinely checked.
In general labs seldom change management
during an asthma exacerbation, especially
a younger patient where a lab draw may actually cause
more respiratory distress.
Imaging such as chest films are unlikely to be helpful
unless an alternative diagnosis, such as pneumothorax,
pneumonia, pneumomediastinum, and atelectasis
are entertained.
Indications for chest X-ray include focal exam findings,
such as crackles or decreased breath sounds,
fever greater than 39 degrees Celsius,
or severe respiratory distress.
An EKG can be considered if severe tachycardia
or electrolyte abnormalities are present.
The goals of treatment include rapid reversal
of airflow obstruction by bronchodilator
and early institution of systemic glucocorticoid.
Correction of hypoxemia and severe hypercapnia, if present,
and correction of dehydration if present.
Interventions include supplemental oxygen
if hypoxemic and IV fluid if there's
evidence of dehydration, such as dry mucous
membranes, poor perfusion, or severe tachycardia.
First-line medications include bronchodilators, most commonly
an inhaled short-acting selective
beta-2 adrenergic agonists, such as albuterol.
Albuterol may be delivered as a nebulizer
at a dose of 0.15 mg/kg, ranging from a minimum of 1.25 mg
and a maximum of 5 mg per dose.
It can also be administered as a metered-dose inhaler
with spacer at a dose of 2 to 8 puffs per dose.
For moderate exacerbation consider
adding a beta-2 agonist combined with ipratropium bromide.
Ipratropium bromide can be given as a dose of 250 mcg per dose
if less than 10 kg or 500 mcg per dose if greater than 10 kg.
Consider three back-to-back inhaled beta-agonist
and ipratropium bromide combine nebulizer
every 20 to 30 minutes.
Point of clarification.
Many institutions use an alternative strategy
that combines the three doses of the beta-agonist
and ipratropium at once over 60 minutes.
This is often referred to as a UniNeb
and decreases potential for interrupted therapy.
For patients with poor inspiratory flow,
or those who cannot cooperate with nebulizer MDI treatment,
alternative first-line therapies may include epinephrine
or terbutaline.
First-line medication also includes
anti-inflammatory systemic glucocorticoid, usually
in the form of prednisone or prednisolone given at 1 to 2
mg/kg at a maximum of 60 mg.
And for those who cannot tolerate oral intake,
consider IV methylprednisolone given at 1 to 2 mg/kg IV
or dexamethasone at 0.6 mg/kg oral IV or IM.
It is important to monitor response to therapy.
Ongoing monitoring every 20 minutes for the first hour
of therapy is required.
This includes monitoring of respiratory rate, heart rate,
oxygen saturation, degree of alertness,
accessory muscle use, retractions,
and chest auscultation.
It is also important to monitor for medication side
effects, such as tachycardia, hypotension, and signs
of electrolyte imbalance.
Failure to respond is indicated by poor air movement, worsening
or persistent hypoxemia, fatigue,
change in mental status, carbon dioxide retention.
If there is failure to respond, it
is important to step up to the next level
of medical treatment.
The indication for an ICU stat, or Code Blue,
include failure to respond to bronchodilator
or systemic steroids, needing albuterol
more often that every two hours, severe hypoxia,
or needing high flow oxygen on the floor, and presence
of hypercarbia, which indicate fatigue and imminent
respiratory failure.
Hemodynamic instability, severe electrolyte imbalance,
asymmetric chest wall movement, tracheal deviation,
and absence of breath sounds, which can all indicate
the presence of a pneumothorax.
If there is no significant response
after three intermittent doses of bronchodilator,
one can consider switching to a continuous albuterol
given at 0.5 mg/kg/hr.
Magnesium sulfate can also be given
IV at a maximum of 2 grams over 20 minutes.
Magnesium sulfate can be administered
alongside with continuous albuterol.
Point of clarification.
Hypotension is a side effect of magnesium.
Consider giving a bolus of normal saline
with or before magnesium administration.
There is no need to check magnesium levels
prior to infusion of magnesium.
If there is again failed response
to continuous albuterol and IV magnesium therapy,
systemic beta-2 agonists can be considered,
such as terbutaline, which can be given at 10 mcg/kg,
subacute.
This may be repeated.
Terbutaline can also be given in IV formulation
of 10 mcg/kg bolus over 10 minutes, followed by infusion.
Epinephrine can also be given at 10
mcg/kg if there is no evidence of anaphylaxis.
This may be repeated.
It is recommended that either terbutaline or epinephrine is
given, but not both.
Point of clarification.
Increased doses of terbutaline greater than 4 mcg/kg/min
are associated with increased risk of side effects,
including tachycardia, hypotension and arrhythmias.
Terbutaline must be given in a monitored setting,
such as the intensive care unit.
If a patient develops hypotension while
on terbutaline, increasing the infusion
by 0.1 to 0.2 mcg/kg/min will help
to overcome the beta-2 selectivity
and improve the hypotension.
There are insufficient data to support
the routine administration of non-standard therapies.
But in patients with life-threatening exacerbations
who are not responding to conventional therapies,
the following may be tried.
Heliox, which is a mixture of helium and oxygen. Please
note that the use of heliox limits the maximum oxygen
concentration delivered.
One can also consider ketamine.
Due to its bronchodilating properties,
this is the drug of choice to provide sedation for anesthesia
before intubating the asthmatic patient.
Point of clarification.
These medications must be given in a monitored setting,
such as the intensive care unit.
Mechanical ventilation.
When possible intubation should be avoided, given potential
to aggravate bronchospasm, induce laryngospasm,
increase barotrauma, and depress circulatory function,
an association with high mortality rate.
Indications for intubations include cardiac or respiratory
arrest, severe hypoxia, and severe hypercapnia
are present, exhaustion, or mental status changes.
Thank you for watching this lecture on asthma respiratory
failure.
Please help us improve the content by providing us
with some feedback.