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Am. J. Respir. Crit. Care Med., Volume 159, Number 1, January 1999, 315-320

Medullary Metastasis Causing Impairment of Respiratory Pressure Output with Intact Respiratory Rhythm

STEPHEN CORNE, KIM WEBSTER, GREGORY MCGINN, WALTER ST.-JOHN, and MAGDY YOUNES

Department of Medicine, University of Manitoba, and Department of Radiology, St. Boniface Hospital, Winnipeg, Canada; and Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire

We present an unusual case of weaning failure. A 67-yr-old man presented with confusion, hyponatremia, and hypercapnic respiratory failure that necessitated mechanical ventilation. CXR revealed a right hilar mass (non-small-cell carcinoma on biopsy). Level of consciousness improved with treatment of his hyponatremia. However, attempts at weaning were complicated by hypercapnia with no overt distress. Resistance and elastance were only slightly abnormal, excluding mechanics as a cause of respiratory failure. Maximal inspiratory pressure (MIP) and vital capacity (VC) were reduced at -15 cm H2O and 0.97 L, respectively. Limb muscle strength was well preserved, suggesting isolated respiratory muscle weakness. During a weaning trial respiratory rate increased from 7 to 40 breaths/min as PCO2 increased from 56 to 89 mm Hg, confirming an intact respiratory pacemaker and good response to CO2. However, spontaneous Pdi was only 1 to 2 cm H2O (< 20% of Pdimax) despite profound hypercapnia. The fact that the patient did not utilize a greater fraction of his pressure-generating capacity suggested preferential impairment of the automatic respiratory centers. MRI showed a large central metastatic lesion in the rostral medulla with only a thin rim of uninvolved tissue. This case illustrates the utility of relating the magnitude of spontaneous efforts to maximal voluntary efforts as a means of localizing the site of involvement in cases of respiratory muscle weakness. It also demonstrates that a large medullary mass lesion may selectively impair brainstem modulation of respiratory pressure output while sparing other medullary functions, and in particular the pacemaking function of the respiratory centers.







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Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 1999 American Thoracic Society
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