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 is unremarkable.
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 – Pathophysiology
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 smoke.
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.
Interventions and Management
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 distress.8
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.
1. Shah MN, Cushman JT, Davis CO, Bazarian JJ, Auinger P, Friedman B. The epidemiology of emergency medical services use by children: an analysis of the National Hospital Ambulatory Medical Care Survey. Prehosp Emerg Care. 2008 Jul-Sep;12(3):269-76.
2. Lerner EB, Dayan PS, Brown K, Fuchs S, Leonard J, Borgialli D, Babcock L, Hoyle JD, Kwok M, Lillis K, Nigrovic LE, Mahajan P, Rogers A, Schwartz H, Soprano J, Tsarouhas N, Turnipseed S, Funai T, Foltin G., Pediatric Emergency Care Applied Research Network (PECARN). Characteristics of the pediatric patients treated by the Pediatric Emergency Care Applied Research Network’s affiliated EMS agencies. Prehosp Emerg Care. 2014 Jan-Mar;18(1):52-9.
3. Adcock IM, Maneechotesuwan K, Usmani O. Molecular interactions between glucocorticoids and long-acting beta2-agonists. J. Allergy Clin. Immunol. 2002 Dec;110(6 Suppl):S261-8.
4. Stead L, Whiteside T. Evaluation of a new EMS asthma protocol in New York City: a preliminary report. Prehosp Emerg Care. 1999 Oct-Dec;3(4):338-42.
5. Knapp B, Wood C. The prehospital administration of intravenous methylprednisolone lowers hospital admission rates for moderate to severe asthma. Prehosp Emerg Care. 2003 Oct-Dec;7(4):423-6.
6. Nassif A, Ostermayer DG, Hoang KB, Claiborne MK, Camp EA, Shah MI. Implementation of a Prehospital Protocol Change For Asthmatic Children. Prehosp Emerg Care. 2018 Jul-Aug;22(4):457-465.
7. Dylla L, Acquisto NM, Manzo F, Cushman JT. Dexamethasone-Related Perineal Burning in the Prehospital Setting: A Case Series. Prehosp Emerg Care. 2018 Sep-Oct;22(5):655-658.
8. Gries DM, Moffitt DR, Pulos E, Carter ER. A single dose of intramuscularly administered dexamethasone acetate is as effective as oral prednisone to treat asthma exacerbations in young children. J. Pediatr. 2000 Mar;136(3):298-303.
9. Meredith, M. (2009, September 30). Attacking Asthma: Five steps to treat pediatric status asthmaticus. Retrieved from: https://www.jems.com/articles/print/volume-34/issue-10/patient-care/attacking-asthma-five-steps-tr.html
10. Hohlfeld, J.M., et.al. (1999). Dysfunction of Pulmonary Surfactant in Asthmatics after Segmental Allergen Challenge. AM J RESPIR CRIT CARE MED (159), 1803–1809.