Acute Myopathy during Treatment of Status Asthmaticus with Corticosteroids and Steroidal Muscle Relaxants

Griffin, Dwayne; Fairman, Nancy; Coursin, Douglas B.; Rawsthorne, Larry; Grossman, Jeffrey E.

doi:10.1378/chest.102.2.510

Cited by 169 publications

(54 citation statements)

References 17 publications

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“…10,11 Several animal and clinical studies have attributed the occurrence of ACM to the use of high doses of corticosteroids in a short period of time. [13][14][15][16][17][18][19][22][23][24] Nava et al, 22 in their rat model, showed that i.v. MP 80 mg/kg/ day for 5 days could induce severe limb and respiratory muscle wasting and predominantly type IIb muscle atrophy.…”

Section: Discussionmentioning

confidence: 99%

“…In human clinical studies, high doses of steroids (up to 3 g/day) are often administered for patients in status asthmaticus or rejection after organ transplantation. 18 ACM has been reported with increased frequency, [13][14][15][16][17][18][19] in patients who have been treated with high-dose corticosteroids since its first description by MacFalane and Rosenthal 24 in 1977. ACM differs from the slowly progressive steroid myopathy described by Cushing 25 in 1932.…”

Section: Discussionmentioning

confidence: 99%

“…12 Procedure and measures Muscle biopsy and electromyography (EMG) were performed for the diagnosis of ACM. [13][14][15][16][17][18][19] Muscle biopsy shows direct evidence of muscle damage from ACM. 20 EMG is an electrodiagnostic study and is performed to confirm ACM from a functional point of view.…”

Section: Subjectsmentioning

confidence: 99%

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High-dose methylprednisolone may cause myopathy in acute spinal cord injury patients

Guo²,

et al. 2004

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Study design: Prospective cohort study. Objective: Although Bracken et al have demonstrated a significant neuroprotective effect of high-dose intravenous (i.v.) methylprednisolone (MP) within 8 h post spinal cord injury (SCI), this practice has recently been challenged. We hypothesized it is possible that acute corticosteroid myopathy (ACM) may occur secondary to the MP. This pilot study was performed to test this hypothesis. Setting: University of Miami School of Medicine/Jackson Memorial Hospital, Miami VA Medical Center, FL, USA. Methods: Subjects included five nonpenetrating traumatic SCI patients, who received 24 h MP according to National Acute Spinal Cord Injury Studies (NASCIS) protocol, and three traumatic patients who suffered SCI and did not receive MP. Muscle biopsies and electromyography (EMG) were performed to determine if myopathic changes existed in these patients. Results: Muscle biopsies from the SCI patients who received 24 h of MP showed muscle damage consistent with ACM in four out of five cases. EMG studies demonstrated myopathic changes in the MP-treated patients. In the three patients who had SCI but did not receive MP, muscle biopsies were normal and EMGs did not reveal evidence of myopathy. Conclusion: Our data suggest that MP in the dose recommended by the NASCIS may cause ACM. If this is true, part of the improvement of neurological recovery showed in NASCIS may be only a recording of the natural recovery of ACM, instead of any protection that MP offers to the injured spinal cord. Sponsorship:

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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High-dose methylprednisolone may cause myopathy in acute spinal cord injury patients

Guo²,

et al. 2004

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“…Finally, the combination of mechanical ventilation with muscle-relaxing agents and/or high-dose steroids was reported to be associated with significant myopathy [19][20][21][22][23]24]. Muscle weakness varied from mildto-severe.…”

Section: Patient Studiesmentioning

confidence: 99%

Effects of mechanical ventilation on diaphragm function and biology

Gayan‐Ramirez¹,

Decramer²

2002

Eur Respir J

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The pathophysiological mechanisms of weaning from mechanical ventilation are not fully known, but there is accumulating evidence that mechanical ventilation induces inspiratory muscle dysfunction.Recently, several animal models have provided potential mechanisms for mechanical ventilation-induced effects on muscle function. In patients, weaning difficulties are associated with inspiratory muscle weakness and reduced endurance capacity. Animal studies demonstrated that diaphragm force was already decreased after 12 h of controlled mechanical ventilation and this worsened with time spent on the ventilator.Diaphragmatic myofibril damage observed after 3-days controlled mechanical ventilation was inversely correlated with maximal diaphragmatic force. Downregulation of the diaphragm insulin-like growth factor-I and MyoD/myogenin messenger ribonucleic acid occurred after 24 h and diaphragmatic oxidative stress and increased protease activity after 18 h. In keeping with these findings, diaphragm fibre atrophy was shown after 12 h and reduced diaphragm mass was reported after 48 h of controlled mechanical ventilation.These animal studies show that early alterations in diaphragm function develop after short-term mechanical ventilation. These alterations may contribute to the difficulties in weaning from mechanical ventilation seen in patients. Strategies to preserve respiratory muscle mass and function during mechanical ventilation should be developed. These may include: adaptation of medication, training of the diaphragm, stabilisation of the catabolic state and pharmacotherapy.

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“…71 This effect can be potentiated by co-administration of high-dose corticosteroids. 72 Determining the cause of diaphragmatic weakness is complicated further because it is a common finding in patients suffering from critical illness polyneuropathy, 73 which is a pervasive phenomenon in patients with sepsis and multi-organ system dysfunction. 74 Approximately 40 -50% of patients who develop ARDS have sepsis as the primary risk factor, [75][76][77][78] which makes the contribution of VIDD to morbidity in patients with ALI/ARDS difficult to determine.…”

Section: Respiratory Muscle Dysfunction and Critical Illness Polyneurmentioning

confidence: 99%

Patient-Ventilator Interaction During Acute Lung Injury, and the Role of Spontaneous Breathing: Part 1: Respiratory Muscle Function During Critical Illness

Kallet

2011

Respir Care

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SummarySince the early 1970s there has been an ongoing debate regarding the wisdom of promoting unassisted spontaneous breathing throughout the course of critical illness in patients with severe respiratory failure. The basis of this debate has focused on the clinical relevance of opposite problems. Historically, the term "disuse atrophy" has described a situation wherein sustained inactivity of the respiratory muscles (ie, passive ventilation) results in deconditioning and weakness. More recently it has been referred to as "ventilator-induced diaphragmatic dysfunction." In contrast, "use atrophy" describes a situation where chronic high-tension inspiratory work causes structural damage to the diaphragm and weakness. Both laboratory and clinical studies demonstrated that relatively brief periods of complete respiratory muscle inactivity, as well as intense muscle loading, result in acute inflammation, loss of muscle mass, and weakness. Yet in critical illness other factors also affect respiratory muscle function, including prolonged use of neuromuscular blocking agents, administration of corticosteroids, and sepsis. This makes the attribution of acquired respiratory muscle weakness and ventilator-dependence to either ventilator-induced diaphragmatic dysfunction or loaded breathing extremely difficult. Regardless, the clinical implications of this research strongly suggest that passive mechanical ventilation should be avoided whenever possible. However, promotion of unassisted spontaneous breathing in the acute phase of critical illness also may carry a substantial risk of respiratory muscle injury and weakness. Use of mechanical ventilation modes in a manner that induces spontaneous breathing effort, while simultaneously reducing the work load on the respiratory muscles, is probably sufficient to minimize both problems. Key words: acute lung injury; acute respiratory distress syndrome; discoordinated breathing; disuse atrophy; respiratory muscle fatigue; ventilator-induced diaphragmatic dysfunction; use atrophy. [Respir Care 2011;56(2):181-189.

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Acute Myopathy during Treatment of Status Asthmaticus with Corticosteroids and Steroidal Muscle Relaxants

Cited by 169 publications

References 17 publications

High-dose methylprednisolone may cause myopathy in acute spinal cord injury patients

High-dose methylprednisolone may cause myopathy in acute spinal cord injury patients

Effects of mechanical ventilation on diaphragm function and biology

Patient-Ventilator Interaction During Acute Lung Injury, and the Role of Spontaneous Breathing: Part 1: Respiratory Muscle Function During Critical Illness

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