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Study Objective: The variable effectiveness of clinical asthma pathways to reduce hospital admissions may be explained in part by the timing of systemic corticosteroid administration. We examine the effect of early (within 60 minutes [SD 15 minutes] of triage) versus delayed (>75 minutes) administration of systemic corticosteroids on health outcomes., Methods: We conducted a prospective observational cohort of children aged 2 to 17 years presenting to the emergency department with moderate or severe asthma, defined as a Pediatric Respiratory Assessment Measure (PRAM) score of 5 to 12. The outcomes were hospital admission, relapse, and length of active treatment; they were analyzed with multivariate logistic and linear regressions adjusted for covariates and potential confounders., Results: Among the 406 eligible children, 88% had moderate asthma; 22%, severe asthma. The median age was 4 years (interquartile range 3 to 8 years); 64% were male patients. Fifty percent of patients received systemic corticosteroids early; in 33%, it was delayed; 17% of children failed to receive any. Overall, 36% of patients were admitted to the hospital. Compared with delayed administration, early administration reduced the odds of admission by 0.4 (95% confidence interval 0.2 to 0.7) and the length of active treatment by 0.7 hours (95% confidence interval -1.3 to -0.8 hours), with no significant effect on relapse. Delayed administration was positively associated with triage priority and negatively with PRAM score., Conclusion: In this study of children with moderate or severe asthma, administration of systemic corticosteroids within 75 minutes of triage decreased hospital admission rate and length of active treatment, suggesting that early administration of systemic corticosteroids may allow for optimal effectiveness., (Copyright © 2012 American College of Emergency Physicians. Published by Mosby, Inc. All rights reserved.)

Emergency medical services (EMS) is an important part of the continuum of asthma management. The magnitude of the EMS responsibility is very large, with millions of patients with asthma treated each year by EMS personnel. In response to inconsistencies between the 1997 National Asthma Education and Prevention Program asthma guidelines and a variety of existing EMS protocols on the management of asthma exacerbations, the Centers for Disease Control and Prevention convened a workgroup in 2004 to discuss the various opportunities and challenges ahead. At the meeting, and over the ensuing year, the workgroup created a model protocol that was derived from the National Asthma Education and Prevention Program guidelines. The model protocol is available in both text and algorithm format and offers guidance for EMS systems to develop and implement treatment protocols in their local areas. The workgroup recommendations emphasize flexibility, simplicity, and low-risk practices. By integrating these recommendations into existing protocols, we believe that EMS systems could improve prehospital care for patients with asthma. Demonstration projects are needed to carefully examine the implementation process and the actual impact of the model protocol on various outcomes. The workgroup also encourages more research on EMS management of asthma exacerbations. In the meantime, improved collaboration between EMS and national asthma organizations is an immediate priority and will continue to advance future discussions on how to improve asthma management in the prehospital setting. The workgroup hopes that state and local EMS systems will see the value of the model protocol and encourage its use.

Status asthmaticus, the most severe form of asthma exacerbation, is a life-threatening condition. The mortality rate in status asthmaticus ranges from 3.5% to 8.3%. Therapeutic approach in acute severe asthma is based on oxygen supply, high doses of nebulised beta2-agonists and systemic corticosteroids administered intravenously or orally. Second line therapy is comprised of methyloxantines, nebulised cholinolitics and management of electrolytes and water balance. Status asthmaticus resulting in acute respiratory failure will often require invasive or non-invasive mechanical ventilation. Mortality in patients with asthma who require mechanical ventilation might exceed 20%. International guidelines for management of status asthmaticus have been published recently, but those recommendations often remain unknown. Thus there is an urgent need for elaboration of national standards on managing acute severe asthma and putting it into clinical practice. Status asthmaticus, especially a severe one, should be treated in a respiratory intermediate intensive care unit.

Objective: To report a case of steroid-induced myopathy resulting from prolonged administration of corticosteroids in an asthmatic patient in a medical intensive care unit., Case Summary: A 30-year-old white man presented with status asthmaticus requiring intubation for respiratory failure. His hospital course was complicated by the need for reintubation and the development of "quadriplegia." Electromyography does not identify neuropathy. After rapid tapering of systemic steroids, the patient quickly regained muscle strength, was extubated, and was transferred to a rehabilitation facility for prolonged physical therapy., Discussion: Steroid-induced myopathy is a rare occurrence in the intensive care setting. Cases of myopathy that have been reported have been associated with prolonged and combined use of corticosteroids with neuromuscular blocking agents or aminoglycosides. Corticosteroids are thought to produce deleterious effects through 1 or all of 3 main pathways: altered electrical excitability of muscle fibers, loss of thick filaments, and/or inhibition of protein synthesis. All of these pathways are believed to increase the rate of muscle catabolism and result in loss of muscle movement., Conclusions: Steroid-induced myopathy is a complication of high-dose steroid use. Unfortunately, in this patient, initial treatment of status asthmaticus required intravenous steroids in high doses to adequately treat the presenting illness. Clinicians should be aware of neuromuscular findings and act aggressively to appropriately eliminate systemic steroids from the treatment regimen.

Background: Since eosinophils are implicated in asthma pathogenesis, we investigated whether these cells were activated in severe asthma., Methods: Twenty-six asthmatics with different clinical responses to oral corticosteroid (CS), i.e. sensitive [change in forced expiratory volume in 1 s (DeltaFEV(1)) >/= 25% after oral methylprednisolone, 40 mg daily, for 14 days, n = 7], resistant (DeltaFEV(1) /= 20 mg oral prednisone daily for acceptable asthma control, n = 10), were studied., Results: Calcium ionophore-induced leukotriene (LT) C(4) release of purified blood eosinophils was similar in the three groups. Cell incubation with granulocyte-macrophage colony-stimulating factor (GM-CSF) enhanced ionophore-induced LTC(4) release, and this effect was higher in CS-sensitive (5-fold) than in CS-resistant subjects (1.7-fold) (p = 0.02). CS treatment decreased blood eosinophil counts in these two groups of subjects (p

We have reviewed the clinical and electrophysiologic features of eleven mechanically ventilated patients with asthma who developed persistent weakness following treatment with neuromuscular blocking agents and corticosteroids. All patients had electrophysiologic findings consistent with a myopathic process and no evidence of a neuromuscular transmission disorder or generalized neuropathy. Electrophysiologic improvement paralleled clinical improvement. The severity of the initial electrophysiologic findings did not predict the subsequent rate of recovery. All patients showed substantial recovery (to functional independence) over the first month.

Skeletal muscle myopathy is one of the main side-effects of systemically administered corticosteroids, and involves respiratory as well as peripheral muscles. After prolonged treatment with moderate doses of either fluorinated or non-fluorinated corticosteroids, chronic myopathy may occur. In patients, such myopathy is characterized by the gradual onset of proximal limb muscle weakness and a sudden increase in creatine excretion in 24h urine. This myopathy is associated with a generalized fiber atrophy of the quadriceps in which myopathic changes are present. Since these changes were also observed in animal models, it was concluded that steroid treatment was responsible for them. After cessation of treatment, recovery of muscle force occurs but may be protracted. The severity of corticosteroid-induced myopathy appears to depend upon the type of steroid used, the treatment duration, the dose and the treatment regimen where repetitive burst treatment effects are worse than those obtained with continuous treatment with the same dose. During short-term treatment with massive doses of corticosteroids as frequently used to treat status asthmaticus, acute myopathy may develop and is characterized by generalized fiber necrosis and rhabdomyolysis. Because such necrosis was not observed in animal studies, it was suggested that the necrosis may result from the combined effect of corticosteroids with other agents such as aminoglycoside antibiotics and/or muscle relaxants.

Acute myopathy in patients being treated for severe asthma has been recognized with increasing frequency since first being described in 1977. We report three patients treated for status asthmaticus who developed severe generalized weakness. Electrophysiologic studies and muscle biopsy revealed evidence of muscle destruction. Each of these patients was treated with high-dose corticosteroids and underwent prolonged neuromuscular blockade with a steroidal muscle relaxant. A review of the literature revealed 15 similar cases. We postulate that the combined effects of corticosteroids and muscle relaxants on the muscle cell may be responsible for this myopathy. Patients treated with corticosteroids and NMBs should be carefully monitored for the development of myopathy.

Patients with severe status asthmaticus who do not respond to intensive medical therapy are often given neuromuscular blocking agents to facilitate mechanical ventilation. Of 51 consecutive asthmatic patients treated with mechanical ventilation, 27 were treated with neuromuscular blocking agents. Of these 27 patients, all receiving high-dose intravenous steroids, four were noted to develop quadriparesis that was more severe distally. There was no cranial nerve or sensory involvement. These four patients were given physical and occupational therapy; three were transferred to the rehabilitation unit. Steady improvement in muscle strength was noted; independence in mobility and activities of daily living was achieved by the time of discharge. They were followed as outpatients until full recovery. Although the exact etiology of the complication is not known, acute steroid myopathy facilitated by the use of neuromuscular blocking agents is a likely cause. Based on the excellent recovery potential of these patients, early rehabilitation in this uncommon complication is strongly urged.

Corticosteroids have been used for over 3 decades in the treatment of asthma. There are theoretic reasons and long-standing clinical support for their use, but little in the way of good objective data on their efficacy. I have reviewed this information and concluded that notwithstanding rare side effects, corticosteroids should be used in acute asthma, and objective data exist to support this premise.