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  • 1
    ISSN: 1432-1238
    Keywords: Muscle relaxants ; Sedation ; Respiratory system mechanics ; Chest wall mechanics ; Mechanical ventilation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To evaluate the separate effects of sedation and paralysis on chest wall and respiratory system mechanics of mechanically ventilated, critically ill patients.Setting: ICU of the University “La Sapienza” Hospital, Rome. Patients and participants 13 critically ill patients were enrolled in this study. All were affected by disease involving both lungs and chest wall mechanics (ARDS in 4 patients, closed chest trauma without flail chest in 4 patients, cardiogenic pulmonary oedema with fluidic overload in 5 patients). Measurements and results Respiratory system and chest wall mechanics were evaluated during constant flow controlled mechanical ventilation in basal conditions (i. e. with the patients under apnoic sedation) and after paralysis with pancuronium bromide. In details, we simultaneously recorded airflow, tracheal pressure, esophageal pressure and tidal volume; with the end-inspiratory and end-expiratory airway occlusion technique we could evaluate respiratory system and chest wall elastance and resistances. Lung mechanics was evaluated by subtracting chest wall from respiratory system data. All data obtained in basal conditions (with the patients sedated with thiopental or propofol) and after muscle paralysis were compared using the Student'st test for paired data. The administration of pancuronium bromide to sedated patients induced a complete muscle paralysis without producing significant modification both to the viscoelastic and to the resistive parameters of chest wall and respiratory system. Conclusions This study demonstrates the lack of additive effects of muscle paralysis in mechanically ventilated, sedated patients. Also in view of the possible side effects of muscle paralysis, our results question the usefulness of generalyzed administration of neuromuscular blocking drugs in mechanically ventilated patients.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1076
    Keywords: Corticosterone methyl oxidase type II ; Failure to thrive ; Salt wasting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Corticosterone methyl oxidase type II (CMO II) deficiency is an uncommon cause of salt-wasting in infancy. We describe a boy who presented with recurrent dehydration and severe failure to thrive in the first 3 months of life, associated with mild hyponatraemia (serum Na+ 127–132 mEq/l) and hyperkalaemia (serum K+ 5.3–5.9 mEq/l). The diagnosis was suggested by an elevated plasma renin activity (PRA): serum aldosterone ratio, and subsequently confirmed by an elevated serum 18-hydroxycorticosterone: aldosterone ratio. Treatment with 9α-fluorohydroxycortisone normalized growth parameters and PRA levels. CMO II deficiency should be considered in infants with recurrent dehydration and failure to thrive, even when serum sodium and potassium levels are not strikingly abnormal.
    Type of Medium: Electronic Resource
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