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LETTERS TO THE EDITOR
tive apneas. The best way to prevent symptoms of hypoventilation is to use noninvasive positive pressure ventilation (at volumes and pressures that greatly alleviate the work of breathing) rather than use CPAP or low span minimally beneficial bi-level PAP. With time, once the investigators’ patients have little or no remaining vital capacity, the CPAP will do them no good and they will either die or, more likely, end up with tracheostomy tubes after a bout of respiratory failure, rather than be introduced to the use of noninvasive aids as needed. The obvious question for Dahan is: How many postpolio or any other patients with neuromuscular respiratory muscle failure do you have who are continuously ventilator dependent and who do not have tracheostomy tubes? If the answer is 1 or more, they should be congratulated but, I fear, that the answer is none so their approach calls for a different evaluationmanagement paradigm.4 John R. Bach, MD Kador Mahajan, BS UMDNJ-New Jersey Medical School, Newark, NJ
[email protected] References 1. Dahan V, Kimoff RJ, Petrof BJ, Benedetti A, Diorio D, Trojan DA. Sleep-disordered breathing in fatigued postpoliomyelitis clinic patients. Arch Phys Med Rehabil 2006;87:1352-6. 2. Bach JR, van der Schans C. The physiological basis of aiding respiratory muscles. In: Bach JR. The management of patients with neuromuscular disease. Philadelphia, Hanley & Belfus; 2004. p 187-210. 3. Filart RA, Bach JR. Pulmonary physical medicine interventions for the elderly with muscular dysfunction. Clin Geriatr Med 2003;19: 189-204. 4. Bach JR. Avoiding respiratory failure in neuromuscular disease: why is it not done? Am J Phys Rehabil 2007;86:222-4.
doi:10.1016/j.apmr.2007.09.022
The authors respond We appreciate the interest and comments of Bach and Mahajan on our study of sleep-disordered breathing (SDB) in fatigued postpoliomyelitis clinic patients.1 Bach has raised important issues in the evaluation and management of postpolio patients with severe pulmonary dysfunction. However, the comments are generally not applicable to our study because pulmonary dysfunction was not severe, on average, in our patient population. We presented the relevant data in table 2 and remarked on it in the Discussion. The mean forced vital capacity for our entire patient population was 91%, and for patients with SDB was also 91%. Mean maximum inspiratory pressure was 85% and mean maximum expiratory pressure was 78% for patients with SDB.1 Patients with this level of pulmonary function do not exhibit the difficulties he mentions. By contrast, we do have a population of neuromuscular disease patients at our center with much more marked pulmonary function abnormalities who undergo either noninvasive or tracheostomy ventilation for isolated nocturnal or sustained diurnal hypoventilation. In our cross-sectional, retrospective study,1 we wanted to alert the clinician caring for patients with previous polio with fatigue that SDB (primarily obstructive sleep hypopnea) is an important, common, and potentially treatable cause of fatigue in this population of patients. Surprisingly, we also found that SDB can occur in patients with previous polio, irrespective of the history of
degree of initial involvement at acute polio (including bulbar and respiratory dysfunction). Therefore, this condition should be considered even in the more general population of postpolio patients, and not just in patients with severe pulmonary dysfunction. Our study objectives, as stated in the introduction, were to determine the frequency (as well as the severity and type) of SDB as well as the predictive factors and symptoms for SDB, and to evaluate the relationship of pulmonary function test measures with oxygen saturation during sleep in fatigued postpolio clinic patients. We believe that we addressed these objectives in the manuscript. Our study objectives did not include providing a review of evaluation and treatment protocols for postpolio patients with severe pulmonary dysfunction. We feel that this was beyond the scope of our study, and refer readers to several excellent reviews on this topic, including those of Bach.2-4 Bach also states that in patients with paradoxical chest wall movement, due to weak chest wall muscles, physicians may falsely attribute these findings to obstructive hypopneas or apneas rather than hypoventilation. We agree that it may be difficult to differentiate between obstructive events and hypoventilation in patients with weak chest wall muscles. However, when respiratory muscles are weak to the point of causing paradoxical thoraco-abdominal movement, this is usually evident not only during sleep but also during wakefulness in the supine body position. Therefore, confusion with obstructive sleep apnea is unlikely. In fact, in our experience, more often the problem is that, in the presence of very weak inspiratory muscles, there is not sufficient negative intrathoracic pressure generation to create the chest wall distortion, which manifests itself as thoraco-abdominal paradox. In such a situation, obstructive hypopneas can actually be underestimated and falsely attributed to central respiratory events or hypoventilation. Daria A. Trojan, MD Diane Diorio, MD Montreal Neurological Institute and Hospital McGill University Montreal, QC, Canada John Kimoff, MD Basil Petrof, MD Respiratory Division and Sleep Laboratory McGill University Health Centre Montreal, QC, Canada Andrea Benedetti, PhD Departments of Medicine and Epidemiology, Biostatistics, and Occupational Health McGill University Montreal, QC, Canada References 1. Dahan V, Kimoff J, Petrof BJ, Benedetti A, Diorio D, Trojan DA. Sleep disordered breathing in fatigued postpoliomyelitis clinic patients. Arch Phys Med Rehabil 2006;87:1352-6. 2. Bach JR, Tilton M. Pulmonary dysfunction and its management in post-polio patients. NeuroRehabilitation 1997;8:139-53. 3. Filiart RA, Bach JR. Pulmonary physical medicine interventions for the elderly patient with muscular dysfunction. Clin Geriatr Med 2003;19:189-204. 4. Perrin C, D’Ambrosio C, White A, Hill NS. Sleep in restrictive and neuromuscular respiratory disorders. Semin Resp Crit Care Med 2005;26:117-30.
doi:10.1016/j.apmr.2007.10.012
Arch Phys Med Rehabil Vol 88, December 2007