Author Credentials and Financial Disclosure: Daniel K. Mullin, MD, is a Clinical Instructor of Emergency Medicine at Drexel University College of Medicine in Philadelphia.
Dr. Mullin has disclosed that he has no financial interests in or relationships with any commercial companies pertaining to this educational activity.
Learning Objectives: After reading this article, the physician should be able to:
- Summarize the various therapeutic options in treating severe acute asthma, and know how and when to use certain treatments.
- Describe the importance of pediatric growth plate injuries.
- Explain the pathophysiology of heat stroke and discuss the therapeutic interventions that should take place.
Release Date: December 2006
State of the Art: Therapeutic Controversies in Severe Acute Asthma
Gibbs MA, et al Acad Emerg Med 2000;7:800
This article was actually a transcript from the 1999 Society for Academic Emergency Medicine state-of-the-art session, “Therapeutic Controversies in Severe Acute Asthma.” All emergency physicians understand that the standard of care for severe acute exacerbations of asthma include beta-agonists and corticosteroids. The purpose of this session was to discuss some of the controversies in delivery methods, doses, and other treatments that may prevent admission to the hospital and assist in preventing some asthmatic patients from respiratory failure and eventual intubation. Much of the material presented was taken from the Cochrane Collaboration and the Multicenter Airway Research Collaboration.
Beta agonists interact with beta receptors on the surface of a variety of cells. Its major effect, relevant to treating asthma, is its ability to relax bronchial smooth muscle. Most emergency physicians give albuterol (a selective beta-2-agonist) in small-volume nebulizers, usually at a dose of 2.5 mg to 5 mg in normal saline.
Practical implications about the use of beta-agonists for treating acute asthma, as discussed in this paper, include that there do not appear to be any data favoring IV beta-agonists over inhaled beta-agonist therapy. That said, the role of IV beta-agonists in addition to inhaled beta-agonists remains unclear. If used, there's some evidence that IV epinephrine appears to be somewhat safe. (Ann Emerg Med 2003;41:706; Ann Emerg Med 2006;47:559.) The article also noted that continuous nebulization of beta-agonists may be more effective than intermittent delivery in severe asthma exacerbations but not mild-to-moderate exacerbations, and that nebulized beta-agonists are no more effective than an MDI with spacer. There is, however, a practical issue because it is easier for physicians and nurses to give a nebulized treatment rather than teaching proper MDI usage, and patients may be upset about receiving the same treatment they were giving themselves at home. The usage of levalbuterol, the R-albuterol isomer (without S-albuterol), was and still is controversial in the emergency treatment of asthma. To date, there are some data to suggest that levalbuterol may decrease the admission rate to hospitals, but there have been methodological flaws, including underdosing of racemic albuterol in these trials. The data are insufficient to recommend levalbuterol in treating acute asthma.
Systemic corticosteroids work by preventing the amplification of the “inflammatory cascade,” and are thought to up-regulate the beta-receptor, resulting in improved bronchodilation. There appears to be short-term and long-term effects in treating asthma, making it a mainstay for acute asthma exacerbations. Using early systemic corticosteroids appears to decrease admission, while in the long run it prevents relapse. The delivery method does not appear relevant. Whether oral, intravenous, or even intramuscular (Chest 2004;126:362), they all appear to be equivalent. The appropriate dose of corticosteroids is unknown at this time, but high-dose corticosteroids (> 360 mg/day of methylprednisolone) offers no advantage over low dose (≤ 80 mg/day). How effective are inhaled corticosteroids in treating acute asthma? There are some data that inhaled flunisolide may improve pulmonary function and decrease the admission rate when used in the acute setting. (Am J Resp Crit Care Med 1998;157:698; Am J Resp Crit Care Med 2005;171:1231.) The jury is still out.
Other treatments for severe asthma, as discussed in this paper, include anticholinergics, magnesium sulfate, heliox, and leukotriene-modifying agents (LMAs). Anticholinergics, specifically nebulized ipratropium bromide, appear to improve pulmonary function and decrease admissions in patients with severe asthma exacerbations. The data supporting nebulized ipratropium are stronger in children, but the current recommendation for adults and children is multiple-dose treatments in the emergency department, particularly for severe asthma exacerbations. Magnesium sulfate also appears to have some utility for asthmatic patients with the most compromised airways. The dose, when given, is 2 g IV over 10 to 20 minutes. In children, the dose is somewhere between 25 mg/kg and 100 mg/kg (max 2 g). The data for heliox and LMAs at the time of this session, and current day, are insufficient to recommend their routine usage in acute, severe asthma exacerbations.
Comment: Asthma treatment has not changed much since the publication of this paper. The mainstays of treatment are beta-agonists and early oral corticosteroids. Because of the many complications of intubating asthmatic patients, emergency physicians should attempt to “throw the kitchen sink” at the patient with impending respiratory failure prior to doing so. This includes nebulized anticholinergics, intravenous magnesium sulfate, subcutaneous, intramuscular, or intravenous beta-agonists, and heliox (if available, rapidly, at a 70:30 or 80:20 mixture). Noninvasive positive pressure ventilation also may be of some utility in those patients who can tolerate them, but the data are much stronger for COPD and CHF exacerbations.
There have been some case reports appearing to support the use of IV ketamine in acute, severe asthma exacerbations to prevent intubation. Larger randomized trials in adults and children do not appear to support these findings, however. (Ann Emerg Med 2005;46:43; Ann Emerg Med 1996;27:170.) Ketamine may be of some utility as an induction agent during rapid sequence intubation of asthmatic patients.
Orthopedic Pitfalls in the ED: Pediatric Growth Plate Injuries
Perron AD, et al Am J Emerg Med 2002;20:50
Orthopedic injuries occur frequently in children and adolescents. Many of these patients first present to the emergency department, and emergency physicians must understand some of the special pitfalls in this population. The most significant difference between the immature skeleton and the mature adult skeletal system is the presence of a physis, or growth plate. This physis is located between the metaphysis and epiphysis of growing bones, and is composed of four distinct zones of proliferating cartilage cells that are fundamental in longitudinal bone growth. Physeal injuries have been reported to account for 15 percent to 30 percent of all skeletal injuries in children, with about 80 percent of these injuries occurring between 10 and 16. Another important difference between adult and children are that the ligaments of children have more relative strength and are more compliant than those of adults. Children rarely suffer from sprains and more frequently suffer fractures, specifically of the physis. Although injuries to the physis rarely cause long-term deficits, missed injuries can lead to premature closure with resultant focal bone growth arrest. For the emergency physician, this is a major cause of malpractice lawsuits.
The Salter-Harris classification system is the most frequently used to describe physeal injuries. The most commonly encountered physeal injury is the Salter-Harris type II injury, accounting for 75 percent of all growth plate injuries. Meanwhile, types III, IV, and V are the injuries which cause the greatest morbidity and the ones that should be evaluated by pediatric orthopedists emergently.
Type I fractures, which most frequently involve infants and toddlers, involve a fracture line through the hypertrophic zone of the physis. Essentially there is a separation of the physis. These usually carry a very good prognosis. Type II fractures have a fracture line through the physis and out through a segment of the metaphysis. The distal radius is the most common site of this injury. These also tend to have a good prognosis. A type III fracture is an intra-articular fracture of the epiphysis with extension through the physis. The prognosis is more guarded. In a type IV fracture, the fracture line originates at the articular surface, crosses the epiphysis, extends through the full thickness of the physis, and exits through a segment of the metaphysis. These occur most frequently in the distal humerus and are at definite risk of growth arrest.
Type V fractures are the least common, luckily accounting for less than one percent of growth plate injuries, but they portend the worst outcomes. They occur most frequently at the knee or ankle, and are caused by compressive forces across the physis, essentially crushing it. These, like Salter-Harris I injuries, are very difficult to diagnose on plain radiographs, and history and physical examination are particularly key. Type V injuries are most often diagnosed in retrospect, when bone growth abnormalities are seen on serial radiographs.
All pediatric patients with point tenderness over a physis and a negative x-ray should be diagnosed with a Salter-Harris type I injury. They should be splinted and referred to an orthopedist. All other Salter-Harris injuries should be splinted as well, but an orthopedist should be called from the emergency department. Patients with type II injuries usually do not need emergency orthopedic evaluation, but patients with types III, IV, or V should be evaluated emergently by a pediatric orthopedist.
Always think twice before writing the diagnosis of “sprain” on the chart or the discharge information of a pediatric patient. These injuries very likely could represent growth plate injuries and so should be treated differently. Additionally, parents should be counseled on the potential for future growth abnormalities, even with minor injuries. Even though it may turn out not to be fractured, this can only be determined by serial radiographs, and we as emergency physicians should be treating the worst case scenario by splinting and giving appropriate follow-up.
Bouchama A, Knochel JP N Engl J Med 2002;346:1978
Heat stroke is a life-threatening illness characterized by an elevated core body temperature that rises above 40°C. It is accompanied by hot, dry skin, and central nervous system abnormalities such as delirium, seizures, or coma. Heat stroke results from exposure to a hot environment (classic or non-exertional) or from strenuous exercise (exertional heat stroke). Data from the Centers for Disease Control and Prevention showed that from 1979 to 1997, 7,000 deaths in the United States were attributable to excessive heat. Most people who are affected by classic heat stroke are very young or very old, poor, socially isolated, and without access to air conditioning.
When one's body temperature is elevated, the heat load must be dissipated by a process called thermoregulation. Peripheral and hypothalamic heat receptors signal the hypothalamic thermoregulatory center that in turn increases the delivery of heated blood to the surface of the body and initiates thermal sweating. An elevated blood temperature also causes tachycardia, increased cardiac output (up to 20 liters per minute), and increased minute ventilation. As the blood is shunted to the periphery, visceral perfusion is reduced, particularly to the kidneys and intestines. Losses of salt and water by sweating, which can amount to greater than two liters per hour, must be balanced by generous salt supplementation to facilitate thermoregulation. Dehydration and salt depletion impair thermoregulation. An inability to increase cardiac output because of salt and water depletion, cardiovascular disease, or a medication that interferes with cardiac function can impair heat tolerance and result in increased susceptibility to heat stroke.
To make the diagnosis of heat stoke, hyperthermia and CNS dysfunction must be present. The core temperature ranges from 40°C to 47°C. Brain dysfunction is usually severe (i.e., coma), but may be subtle, manifesting as altered judgment or inappropriate behavior. Seizures may occur, especially during cooling. Heat stroke can progress to multi-organ dysfunction, causing acute renal failure, DIC, ARDS, intestinal ischemia, myocardial infarction, etc.
When diagnosed, treatment should begin immediately and consists, first and foremost, of external cooling. These authors recommended cooling by removing all clothes, placing cold packs on the neck, axillae, and groin, continuous fanning, and spraying the skin with tepid water. Some experts recommended packing the heat stroke patient in ice or immersing in ice water, but evaporative cooling has been proven in several studies to be approximately two times faster. (J App Physiol 1959;14:771; Lancet 1980;1:507.) Intubation should be considered if the patient is not protecting his airway. Isotonic crystalloids should be given via intravenous bolus, and benzodiazepines should be given for seizures. Rhabdomyolysis should be treated as per standard protocol, and electrolytes, especially serum potassium, should be closely monitored.
Early recovery of central nervous system function during cooling is a favorable prognostic indicator. Meanwhile, up to 20 percent of patients may end up with residual brain damage.
About the LLSA
As part of its continuous certification program, the American Board of Emergency Medicine has developed the Lifelong Learning and Self-Assessment (LLSA) program to promote continuous education of diplomates. Each year, beginning in 2004, 16 to 20 articles are chosen based on the Emergency Medicine Model. A list of these articles can be found on the ABEM web site, www.abem.org.
ABEM is not authorized to confer CME credit for the successful completion of the LLSA test, but it has no objection to physicians participating in such activities. EMN's CME activity, Learning to Live with the LLSA, is not affiliated with ABEM's LLSA program, and reading this article and completing the quiz does not count toward ABEM certification. Rather, participants may earn 1 CME credit from the Lippincott Continuing Medical Education Institute, Inc., for each completed EMN quiz.