EMS responds to a residence for a seven-year-old male with a\ncough and trouble breathing. This episode began two hours ago and has been\naccompanied by a runny nose without any other symptoms. His mother has been\ntreating him with albuterol by a nebulizer, but he has progressively become\nmore short of breath. Past medical history\nis notable for asthma since infancy, with multiple prior hospitalizations. Physically, the patient appears to be in\nmoderate respiratory distress, with obvious nasal flaring, suprasternal and\nintercostal retractions. His vital signs include a respiratory rate of 40\/minute,\nheart rate of 120\/minute, and pulse oximetry of 93 percent on room air. Lung\nexam is notable for diffuse inspiratory and expiratory bilateral wheezing, poor\nair movement and a prolonged expiratory phase. The remainder of the examination\nis unremarkable.<\/p>\n\n\n\n
What is significant about his presentation and assessment\nfindings? What are your management\nstrategies? How sick is this child and\nwill he get worse? These are questions\nthat have to be answered in a timely manner; even more so when it involves a\npediatric patient. Let\u2019s discuss what is\nhappening to him and what EMS professionals can do in the prehospital setting.<\/p>\n\n\n\n
Case Discussion –\nPathophysiology<\/strong><\/p>\n\n\n\n Asthma is a common chronic childhood disease, and a frequent reason for pediatric\nemergency medical treatment. It affects approximately 10-15 percent of\nall children in the United States.1<\/sup> Risk factors include obesity,\npremature birth and a chronic environmental exposure to pollutants. Some children are genetically predisposed, as\nasthma tends to be passed down through generations. An acute asthma attack is commonly\nprecipitated by factors such as an allergen exposure, stress, exercise, food\nadditives, recent upper respiratory infections, exposure to cold air or tobacco\nsmoke.<\/p>\n\n\n\n EMS professionals need to keep in mind that a child\u2019s lower\nairway anatomy is proportionally smaller than an adult, and is easily\ncompromised from lesser degrees of swelling and constriction. In response to one of the aforementioned\nevents, a series of reactions occur in the lower airway. First, the smooth\nmuscle surrounding the bronchioles is stimulated by histamine and leukotriene, causing\nbronchoconstriction. Secondly, mucous glands and cells that line the lower\nairway are stimulated to secrete excessive mucous, which plugs the bronchioles.\nFinally, fluid shifts into the walls of the lower airway, resulting in inflammation\nand decrease in airway diameter. The net result is a narrowing of the small\nairways with increased resistance to airflow. \n<\/p>\n\n\n\n These pathophysiologic changes cause distal alveoli to trap\nair and become hyper-inflated. As the amount\nof hyper-inflated lung tissue increases, the child\u2019s diaphragm is progressively\nflattened, causing a mechanical disruption of ventilation. The increasing workload to ventilate is\ntransferred onto the smaller and weaker intercostal and suprasternal muscles. Once these muscles rapidly fatigue from\nstress and overuse, the onset of respiratory failure is quick. Air trapping not only increases\nintra-thoracic pressure but also directly puts pressure on the child\u2019s heart \u2013\nsimilar to the mechanics of a cardiac tamponade. Physical compression of the superior and\ninferior vena cava also occurs. The result is a lesser-than-normal amount of\navailable blood return into the right atrium – reducing right ventricular\nfilling, and systolic output. Coupled with this lack of volume, the heart has\nto force blood against an increased pulmonary artery pressure. This is due to pulmonary capillary\ncompression from the surrounding hyper-inflated lung tissue. The acute pulmonary\nhypertension expedites the acute right ventricular failure, poor perfusion to\nany remaining functional alveoli, and hypoxemia. <\/p>\n\n\n\n Hypoxemia also develops from collapsed alveoli. They are still being perfused, but are unable\nto participate in gas exchange. Blood flows through capillaries adjacent to the\ncollapsed alveoli and returns to the left side of the heart, still deoxygenated. A working hypothesis as to why the alveoli\ncollapse suggests that a lack of alveolar surfactant develops when the asthma immune\nresponse shuts down the surfactant cells. Once the amount of surfactant is\ninsufficient to lower the surface tension between the alveoli and capillaries,\nthe alveoli collapse. In addition,\npulmonary surfactant is essential to maintain patency of the\nterminal\/respiratory bronchioles.10<\/sup> Lack of surfactant causes those\nairways to collapse and become temporarily blocked, adding to the air trapping.<\/p>\n\n\n\n The increased ventilation rate in the distressed child accelerates\nvolume loss, decreasing perfusion to multiple organ systems. This, combined with the resultant hypoxia,\nleads to cellular anaerobic metabolism and systemic accumulation of lactic acid\nand ketones. Once respiratory failure\noccurs, these by-products combine with increased levels of carbon dioxide to profoundly\ndecrease serum pH and hasten the rapid onset of respiratory arrest, followed\nquickly by cardiac arrest.<\/p>\n\n\n\n Patient Presentation<\/strong><\/p>\n\n\n\n During an acute attack, varying degrees of dyspnea,\ntachypnea, tachycardia, accessory muscle use, retractions, coughing, jugular\nvenous distention, audible wheezing, skin color, hyper-resonant lung sounds and\nmental status changes manifest. Bronchiolitis may mimic asthma in children\nyounger than two years of age, and wheezing can be a sign of foreign body\ningestion in toddlers.2<\/sup> Providers should observe the patient\u2019s work\nof breathing as well as auscultate for abnormal lung sounds. The lack of\nabnormal lung sounds may be an ominous sign of poor air movement in a patient\nat risk for respiratory failure. Pertinent items from the patient\u2019s history\ninclude prior diagnosis of asthma, onset, and triggers for the exacerbation,\ncurrent asthma medications, and prior ED visits or hospitalizations for asthma\n(including intensive care unit admissions and\/or intubations).<\/p>\n\n\n\n As a baseline, an acute asthma attack presents with a degree\nof respiratory distress. The presence of wheezing often characterizes the\nseverity of the attack, and thus, the degree of bronchoconstriction. In a mild\nasthma attack, wheezing is typically audible at the end of expiration,\nindicating increased resistance to expiratory airflow. Oxygen saturation levels\nmay be normal or slightly low. During a\nmore severe asthma attack, wheezing may be audible during inspiration and\nexpiration, or may disappear completely. Oxygen saturation levels typically\nreflect hypoxemia, with readings that usually range from less than 90 to 94\npercent. Characteristically, as lower airway\nobstruction worsens, capnography waveforms develop a raised \u201cshark-fin\u201d shape. This\nshape progressively flattens toward the baseline if airway patency and\nsufficient airflow is not restored. <\/p>\n\n\n\n Status asthmaticus is a life-threatening condition of\nprogressively-worsening bronchospasm and respiratory dysfunction due to asthma,\nunresponsive to conventional therapy. It\ntypically progresses into respiratory failure and arrest and requires\naggressive ventilatory and pharmacological interventions. The child with status\nasthmaticus presents with air hunger. Because of the profound bronchoconstriction\nand minimal airflow through the bronchioles, wheezing is either faint or\ncompletely absent. Oxygen saturation levels often reflect severe hypoxia, with\nreadings well below 90 percent. During an ongoing and unbroken asthma attack, the\nchild becomes profoundly acidotic from retained carbon dioxide, mainly due to\npoor inspiratory and expiratory effort and diminished air movement through the lower\nairways. This may initially manifest as\nan increased respiratory rate. If\nuncorrected, though, the respiratory rate will decrease, possibly giving the\nEMS professional a feeling that the patient is getting better. The fact is, the child is tiring and is\ntransitioning from respiratory distress into respiratory failure.<\/p>\n\n\n\n Interventions and\nManagement<\/strong><\/p>\n\n\n\n Once the EMS professional concludes the most likely\ndiagnosis is an asthma exacerbation, treatment should be centered around correcting\nhypoxemia, reversing bronchoconstriction and airway inflammation, rehydration\nand monitoring for complications – such as pneumothorax. <\/p>\n\n\n\n Hypoxia is the number one killer of asthmatic patients. Thus, first-line treatment of a patient with\nany degree of respiratory distress should be oxygen administration by the most\nefficient delivery method. Not only does\nit help reverse the patient\u2019s hypoxemia, but oxygen also acts as a\nbronchodilator \u2013 helping to open the lower airways.9<\/sup> Albuterol is the other mainstay medication\nfor asthma patients by its ability to relax bronchial smooth muscle and enhance\nmucous clearance. It may be administered\nconcurrently with oxygen, but should never delay oxygen administration.\nIdeally, albuterol is a nebulized solution (2.5 milligrams (mg) per dose for\npatients less than 10 kilograms (kg), and 5 mg per dose for patients greater\nthan 10 kg). Common side effects include tachycardia and tremors. Rarely, children may experience arrhythmias\nsuch as supraventricular tachycardia. The addition of ipratropium bromide (0.5\nmg per dose) to albuterol has been shown to positively influence a child\u2019s\noutcome. The combination of ipratropium bromide and albuterol may be repeated,\nas needed, for persistent respiratory distress. 3,4,5,6,7<\/sup> <\/p>\n\n\n\n For critically ill children and those in status, several\nother adjunctive therapies should be considered. Early administration of corticosteroids\nin addition to inhaled beta-2-agonists is recommended, typically at a dose of 2\nmg\/kg. Additionally, intravenous magnesium has been noted to produce positive\nbronchodilation effects within pediatric patients suffering from status\nasthmaticus. It is dosed at 50 mg\/kg IV\nover 10-20 minutes. Common side effects\ninclude skin flushing and hypotension, which is rarely clinically significant\nand responds well to fluid administration. <\/p>\n\n\n\n Pediatric patients in prolonged status asthmaticus may\nrequire further aggressive treatment with epinephrine. The intramuscular route is preferred and the\nmedication should be injected into the pediatric patient\u2019s lateral thigh. The\nproper dose is 0.01 mg\/kg (0.1 mL\/kg), using a 1:1000 concentration. Life-saving therapy with intravenous\nepinephrine may be indicated for patients who don\u2019t improve with intramuscular\nepinephrine and intravenous magnesium, but only if carefully done. <\/p>\n\n\n\n Intravenous epinephrine must be given very cautiously and\nslowly. Never give it as a push\/bolus. \nAdd one milligram of epinephrine (1:1000) to an IV bag of 250 mL saline\nor D5<\/sub>W, and run this infusion through a micro drip chamber drop set,\nstarting at 15 drops per minute. Piggyback this slow drip into a high-flow IV\nmainline so it gets into the patient’s circulation as quickly as possible. Recheck\nthe patient for desired effects at one-minute intervals. Slow or discontinue\nthe drip as the patient improves or if cardiac toxicity occurs.9<\/sup><\/p>\n\n\n\n Mechanical ventilation may be necessary, in rare cases. Non-invasive\nventilation with bi-level positive airway pressure (BiPAP) can help stave off\nintubation and preserves the conscious patient\u2019s respiratory drive. Intubation\nand mechanical ventilation are the last resort for patients with\nrefractory respiratory failure and\/or respiratory arrest. Consider ketamine\nadministration if sedating prior to intubation. \nIntravenous ketamine with doses starting at 2 mg\/kg, is gaining favor as\nan adjunctive bronchodilator, especially for agitated patients in respiratory\ndistress.8<\/sup><\/p>\n\n\n\n The effects of positive pressure ventilation on the\ncardiovascular system are well known. In normal breathing, the negative pressure\nphase of inspiration assists venous return, alleviates pressure on the\npulmonary capillaries, and encourages flow. With positive pressure ventilation,\nthe intrathoracic pressure increases during inspiration causing a decrease in\nvenous return, right ventricular output, and pulmonary blood flow. Remember, this is already occurring in the\nasthmatic patient from lung hyperinflation. \nVentilate with lower rates and tidal volumes to provide enough time for\nthe patient to exhale. This will not\nonly delay the increase in intrathoracic pressure, but also help to avoid\nbarotrauma and increasing workload on the patient\u2019s heart.<\/p>\n\n\n\n ______________________________________________________________________________<\/p>\n\n\n\n References<\/p>\n\n\n\n 1. Shah MN, Cushman JT, Davis CO, Bazarian\nJJ, Auinger P, Friedman B. The epidemiology of emergency medical services use\nby children: an analysis of the National Hospital Ambulatory Medical Care\nSurvey. Prehosp Emerg Care. 2008 Jul-Sep;12(3):269-76.<\/p>\n\n\n\n 2. Lerner EB, Dayan PS, Brown K, Fuchs\nS, Leonard J, Borgialli D, Babcock L, Hoyle JD, Kwok M, Lillis K, Nigrovic LE,\nMahajan P, Rogers A, Schwartz H, Soprano J, Tsarouhas N, Turnipseed S, Funai T,\nFoltin G., Pediatric Emergency Care Applied Research Network (PECARN).\nCharacteristics of the pediatric patients treated by the Pediatric Emergency\nCare Applied Research Network’s affiliated EMS agencies. Prehosp Emerg Care.\n2014 Jan-Mar;18(1):52-9.<\/p>\n\n\n\n 3. Adcock IM, Maneechotesuwan K, Usmani\nO. Molecular interactions between glucocorticoids and long-acting\nbeta2-agonists. J. Allergy Clin. Immunol. 2002 Dec;110(6 Suppl):S261-8. <\/p>\n\n\n\n 4. Stead L, Whiteside T. Evaluation of\na new EMS asthma protocol in New York City: a preliminary report. Prehosp Emerg\nCare. 1999 Oct-Dec;3(4):338-42. <\/p>\n\n\n\n 5. Knapp B, Wood C. The prehospital\nadministration of intravenous methylprednisolone lowers hospital admission\nrates for moderate to severe asthma. Prehosp Emerg Care. 2003\nOct-Dec;7(4):423-6.<\/p>\n\n\n\n 6. Nassif A, Ostermayer DG, Hoang KB,\nClaiborne MK, Camp EA, Shah MI. Implementation of a Prehospital Protocol Change\nFor Asthmatic Children. Prehosp Emerg Care. 2018 Jul-Aug;22(4):457-465. <\/p>\n\n\n\n 7. Dylla L, Acquisto NM, Manzo F,\nCushman JT. Dexamethasone-Related Perineal Burning in the Prehospital Setting:\nA Case Series. Prehosp Emerg Care. 2018 Sep-Oct;22(5):655-658.<\/p>\n\n\n\n 8. Gries DM, Moffitt DR, Pulos E,\nCarter ER. A single dose of intramuscularly administered dexamethasone acetate\nis as effective as oral prednisone to treat asthma exacerbations in young\nchildren. J. Pediatr. 2000 Mar;136(3):298-303.<\/p>\n\n\n\n