EMS responds to a residence for a seven-year-old male with a
cough and trouble breathing. This episode began two hours ago and has been
accompanied by a runny nose without any other symptoms. His mother has been
treating him with albuterol by a nebulizer, but he has progressively become
more short of breath. Past medical history
is notable for asthma since infancy, with multiple prior hospitalizations. Physically, the patient appears to be in
moderate respiratory distress, with obvious nasal flaring, suprasternal and
intercostal retractions. His vital signs include a respiratory rate of 40/minute,
heart rate of 120/minute, and pulse oximetry of 93 percent on room air. Lung
exam is notable for diffuse inspiratory and expiratory bilateral wheezing, poor
air movement and a prolonged expiratory phase. The remainder of the examination
What is significant about his presentation and assessment
findings? What are your management
strategies? How sick is this child and
will he get worse? These are questions
that have to be answered in a timely manner; even more so when it involves a
pediatric patient. Let’s discuss what is
happening to him and what EMS professionals can do in the prehospital setting.
Case Discussion –
Asthma is a common chronic childhood disease, and a frequent reason for pediatric
emergency medical treatment. It affects approximately 10-15 percent of
all children in the United States.1 Risk factors include obesity,
premature birth and a chronic environmental exposure to pollutants. Some children are genetically predisposed, as
asthma tends to be passed down through generations. An acute asthma attack is commonly
precipitated by factors such as an allergen exposure, stress, exercise, food
additives, recent upper respiratory infections, exposure to cold air or tobacco
EMS professionals need to keep in mind that a child’s lower
airway anatomy is proportionally smaller than an adult, and is easily
compromised from lesser degrees of swelling and constriction. In response to one of the aforementioned
events, a series of reactions occur in the lower airway. First, the smooth
muscle surrounding the bronchioles is stimulated by histamine and leukotriene, causing
bronchoconstriction. Secondly, mucous glands and cells that line the lower
airway are stimulated to secrete excessive mucous, which plugs the bronchioles.
Finally, fluid shifts into the walls of the lower airway, resulting in inflammation
and decrease in airway diameter. The net result is a narrowing of the small
airways with increased resistance to airflow.
These pathophysiologic changes cause distal alveoli to trap
air and become hyper-inflated. As the amount
of hyper-inflated lung tissue increases, the child’s diaphragm is progressively
flattened, causing a mechanical disruption of ventilation. The increasing workload to ventilate is
transferred onto the smaller and weaker intercostal and suprasternal muscles. Once these muscles rapidly fatigue from
stress and overuse, the onset of respiratory failure is quick. Air trapping not only increases
intra-thoracic pressure but also directly puts pressure on the child’s heart –
similar to the mechanics of a cardiac tamponade. Physical compression of the superior and
inferior vena cava also occurs. The result is a lesser-than-normal amount of
available blood return into the right atrium – reducing right ventricular
filling, and systolic output. Coupled with this lack of volume, the heart has
to force blood against an increased pulmonary artery pressure. This is due to pulmonary capillary
compression from the surrounding hyper-inflated lung tissue. The acute pulmonary
hypertension expedites the acute right ventricular failure, poor perfusion to
any remaining functional alveoli, and hypoxemia.
Hypoxemia also develops from collapsed alveoli. They are still being perfused, but are unable
to participate in gas exchange. Blood flows through capillaries adjacent to the
collapsed alveoli and returns to the left side of the heart, still deoxygenated. A working hypothesis as to why the alveoli
collapse suggests that a lack of alveolar surfactant develops when the asthma immune
response shuts down the surfactant cells. Once the amount of surfactant is
insufficient to lower the surface tension between the alveoli and capillaries,
the alveoli collapse. In addition,
pulmonary surfactant is essential to maintain patency of the
terminal/respiratory bronchioles.10 Lack of surfactant causes those
airways to collapse and become temporarily blocked, adding to the air trapping.
The increased ventilation rate in the distressed child accelerates
volume loss, decreasing perfusion to multiple organ systems. This, combined with the resultant hypoxia,
leads to cellular anaerobic metabolism and systemic accumulation of lactic acid
and ketones. Once respiratory failure
occurs, these by-products combine with increased levels of carbon dioxide to profoundly
decrease serum pH and hasten the rapid onset of respiratory arrest, followed
quickly by cardiac arrest.
During an acute attack, varying degrees of dyspnea,
tachypnea, tachycardia, accessory muscle use, retractions, coughing, jugular
venous distention, audible wheezing, skin color, hyper-resonant lung sounds and
mental status changes manifest. Bronchiolitis may mimic asthma in children
younger than two years of age, and wheezing can be a sign of foreign body
ingestion in toddlers.2 Providers should observe the patient’s work
of breathing as well as auscultate for abnormal lung sounds. The lack of
abnormal lung sounds may be an ominous sign of poor air movement in a patient
at risk for respiratory failure. Pertinent items from the patient’s history
include prior diagnosis of asthma, onset, and triggers for the exacerbation,
current asthma medications, and prior ED visits or hospitalizations for asthma
(including intensive care unit admissions and/or intubations).
As a baseline, an acute asthma attack presents with a degree
of respiratory distress. The presence of wheezing often characterizes the
severity of the attack, and thus, the degree of bronchoconstriction. In a mild
asthma attack, wheezing is typically audible at the end of expiration,
indicating increased resistance to expiratory airflow. Oxygen saturation levels
may be normal or slightly low. During a
more severe asthma attack, wheezing may be audible during inspiration and
expiration, or may disappear completely. Oxygen saturation levels typically
reflect hypoxemia, with readings that usually range from less than 90 to 94
percent. Characteristically, as lower airway
obstruction worsens, capnography waveforms develop a raised “shark-fin” shape. This
shape progressively flattens toward the baseline if airway patency and
sufficient airflow is not restored.
Status asthmaticus is a life-threatening condition of
progressively-worsening bronchospasm and respiratory dysfunction due to asthma,
unresponsive to conventional therapy. It
typically progresses into respiratory failure and arrest and requires
aggressive ventilatory and pharmacological interventions. The child with status
asthmaticus presents with air hunger. Because of the profound bronchoconstriction
and minimal airflow through the bronchioles, wheezing is either faint or
completely absent. Oxygen saturation levels often reflect severe hypoxia, with
readings well below 90 percent. During an ongoing and unbroken asthma attack, the
child becomes profoundly acidotic from retained carbon dioxide, mainly due to
poor inspiratory and expiratory effort and diminished air movement through the lower
airways. This may initially manifest as
an increased respiratory rate. If
uncorrected, though, the respiratory rate will decrease, possibly giving the
EMS professional a feeling that the patient is getting better. The fact is, the child is tiring and is
transitioning from respiratory distress into respiratory failure.
Once the EMS professional concludes the most likely
diagnosis is an asthma exacerbation, treatment should be centered around correcting
hypoxemia, reversing bronchoconstriction and airway inflammation, rehydration
and monitoring for complications – such as pneumothorax.
Hypoxia is the number one killer of asthmatic patients. Thus, first-line treatment of a patient with
any degree of respiratory distress should be oxygen administration by the most
efficient delivery method. Not only does
it help reverse the patient’s hypoxemia, but oxygen also acts as a
bronchodilator – helping to open the lower airways.9 Albuterol is the other mainstay medication
for asthma patients by its ability to relax bronchial smooth muscle and enhance
mucous clearance. It may be administered
concurrently with oxygen, but should never delay oxygen administration.
Ideally, albuterol is a nebulized solution (2.5 milligrams (mg) per dose for
patients less than 10 kilograms (kg), and 5 mg per dose for patients greater
than 10 kg). Common side effects include tachycardia and tremors. Rarely, children may experience arrhythmias
such as supraventricular tachycardia. The addition of ipratropium bromide (0.5
mg per dose) to albuterol has been shown to positively influence a child’s
outcome. The combination of ipratropium bromide and albuterol may be repeated,
as needed, for persistent respiratory distress. 3,4,5,6,7
For critically ill children and those in status, several
other adjunctive therapies should be considered. Early administration of corticosteroids
in addition to inhaled beta-2-agonists is recommended, typically at a dose of 2
mg/kg. Additionally, intravenous magnesium has been noted to produce positive
bronchodilation effects within pediatric patients suffering from status
asthmaticus. It is dosed at 50 mg/kg IV
over 10-20 minutes. Common side effects
include skin flushing and hypotension, which is rarely clinically significant
and responds well to fluid administration.
Pediatric patients in prolonged status asthmaticus may
require further aggressive treatment with epinephrine. The intramuscular route is preferred and the
medication should be injected into the pediatric patient’s lateral thigh. The
proper dose is 0.01 mg/kg (0.1 mL/kg), using a 1:1000 concentration. Life-saving therapy with intravenous
epinephrine may be indicated for patients who don’t improve with intramuscular
epinephrine and intravenous magnesium, but only if carefully done.
Intravenous epinephrine must be given very cautiously and
slowly. Never give it as a push/bolus.
Add one milligram of epinephrine (1:1000) to an IV bag of 250 mL saline
or D5W, and run this infusion through a micro drip chamber drop set,
starting at 15 drops per minute. Piggyback this slow drip into a high-flow IV
mainline so it gets into the patient’s circulation as quickly as possible. Recheck
the patient for desired effects at one-minute intervals. Slow or discontinue
the drip as the patient improves or if cardiac toxicity occurs.9
Mechanical ventilation may be necessary, in rare cases. Non-invasive
ventilation with bi-level positive airway pressure (BiPAP) can help stave off
intubation and preserves the conscious patient’s respiratory drive. Intubation
and mechanical ventilation are the last resort for patients with
refractory respiratory failure and/or respiratory arrest. Consider ketamine
administration if sedating prior to intubation.
Intravenous ketamine with doses starting at 2 mg/kg, is gaining favor as
an adjunctive bronchodilator, especially for agitated patients in respiratory
The effects of positive pressure ventilation on the
cardiovascular system are well known. In normal breathing, the negative pressure
phase of inspiration assists venous return, alleviates pressure on the
pulmonary capillaries, and encourages flow. With positive pressure ventilation,
the intrathoracic pressure increases during inspiration causing a decrease in
venous return, right ventricular output, and pulmonary blood flow. Remember, this is already occurring in the
asthmatic patient from lung hyperinflation.
Ventilate with lower rates and tidal volumes to provide enough time for
the patient to exhale. This will not
only delay the increase in intrathoracic pressure, but also help to avoid
barotrauma and increasing workload on the patient’s heart.
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