Chest
Volume 101, Issue 5, May 1992, Pages 1413-1416
Journal home page for Chest

Prolonged Neurogenic Weakness in Patients Requiring Mechanical Ventilation for Acute Airflow Limitation

https://doi.org/10.1378/chest.101.5.1413Get rights and content

We describe three patients who required mechanical ventilation for severe acute exacerbations of obstructive airways disease. When treatment with sedatives and muscle relaxants was withdrawn, they exhibited profound generalized weakness and consequently required prolonged ventilation despite resolution of the airway obstruction. Clinical features were variable, but none of the patients developed failure of other organs and infection was confined to the lungs. All had electrophysiologic evidence of a predominantly motor axonal syndrome. One patient in whom sensory action potentials were abnormal may represent an unusually severe case of critical illness neuropathy occurring in the absence of systemic sepsis and multiple organ failure. In the other two cases, this diagnosis is made less likely by the complete absence of sensory involvement and in these patients the lesion appeared to be either in the most distal portion of the motor neuron or at the neuromuscular junction. In all three patients, resolution was slow but eventually complete. The etiology of the condition is not clear, but it seems to be distinct from the acute myopathy previously described in asthmatics who had received mechanical ventilation. It is important to recognize this phenomenon to avoid erroneous conclusions about the likelihood of the patient recovering from ventilator dependence. A prolonged weaning period is to be expected in such cases.

Section snippets

CASE 1

A 41-year-old male nonsmoker with long-standing asthma had become increasingly breathless despite increasing his oral prednisolone dosage from 10 mg to 40 mg daily. At the time of hospital admission, he was dyspneic, wheezy, and sweating, with a pulse rate of 140 beats/min. Nebulized salbutamol, intravenous aminophylline, and hydrocortisone failed to prevent deterioration and mechanical ventilation was instituted. He received intravenous infusions of salbutamol, aminophylline, hydrocortisone,

DISCUSSION

There have been several reports of weakness in patients requiring mechanical ventilation for acute severe asthma.1, 2, 3, 4, 5 These patients typically presented with weaning difficulties and flaccid weakness affecting both proximal and distal muscle groups with preserved tendon reflexes and without sensory involvement. All had received intravenous sedatives and muscle relaxants together with specific medication for airway obstruction, including bronchodilators and steroids. Initial reports

ACKNOWLEDGMENT

We would like to thank Dr. R. W. H. Walker and Dr. J. D. Watson for their helpful advice and criticism.

REFERENCES (11)

  • MacFarlaneIA et al.

    Severe myopathy after status asthmaticus

    Lancet

    (1977)
  • KupferY et al.

    Disuse atrophy in a ventilated patient with status asthmaticus receiving neuromuscular blockade

    Crit Care Med

    (1987)
  • BachmannP et al.

    Hydrocortisone and pancuronium bromide: acute myopathy during status asthmaticus

    Crit Care Med

    (1988)
  • KnoxAJ et al.

    Acute hydrocortisone myopathy in acute severe asthma

    Thorax

    (1986)
  • Van MarieW et al.

    Acute hydrocortisone myopathy

    BMJ

    (1980)
There are more references available in the full text version of this article.

Cited by (52)

  • Corticosteroids and neuromuscular blockers in development of critical illness neuromuscular abnormalities: A historical review

    2017, Journal of Critical Care
    Citation Excerpt :

    Over the next 2 decades, numerous case reports and small case series (<15 patients) of flaccid paralysis after ICU admission followed [31,32]. Many of these cases reported on simultaneous use of high-dose corticosteroids and 6 or more days of continuous infusions of steroidal NMB [6-12,33-40], but not all patients were treated with NMB [4,5,32,33,41]. Many of these accounts appear to be describing critical illness myopathy syndromes, with EMGs demonstrating myopathic abnormalities [9,12,32,34,35,40,41] and elevations in CK levels [8,9,34,40].

  • The Respiratory System and Neuromuscular Diseases

    2015, Murray and Nadel's Textbook of Respiratory Medicine: Volume 1,2, Sixth Edition
  • Clinical aspects of respiratory muscle dysfunction in the critically ill

    2001, Chest
    Citation Excerpt :

    Although Clarence Olsen94 reported in 1956 thatperipheral nerve lesions could complicate a variety of criticalillnesses, systematic studies have been undertaken only relativelyrecently. The reported studies fall into the following two main groups:those that study unselected ICU patients with prolonged hospitaladmissions or features of multiorgan dysfunction9596979899100101102;and those that study patients with clinical features suggestive of neurologic abnormalities103104105106107108109 or with specificdiagnoses.110111112 In addition, reported studies have useda variety of investigational techniques and definitions to report thedata.

  • Weaning from mechanical ventilation

    1999, Journal of Critical Care
  • Muscle dysfunction in the intensive care unit

    1999, Clinics in Chest Medicine
View all citing articles on Scopus
View full text