Canadian Neighbor Pharmacy: Discussion of Nasal Intermittent Positive Pressure Ventilation in Patients With Obesity-Hypoventilation Syndrome
Obesity can have detrimental effects on respiratory function, and it may lead to chronic hypoventilation in some patients. Why some obese patients develop OHS while others breathe normally remains speculative. Contributing factors may include the restrictive pulmonary function defect, increased work of breathing and CO2 production, and altered central respiratory control.- Some available data support a possible role for airway obstruction in the pathogenesis of diurnal hypercapnia in certain patients with OHS and SAS, although this finding has not been confirmed in other studies. We think that most authors would exclude patients with significant COPD from the diagnosis of OHS, and, in this article, we have only considered those patients who did not have an obstructive ventilatory defect, as measured by spirometry. On the other hand, OHS and SAS have frequently been associated,2 and it is not fully understood whether there is a role for SAS in the pathogenesis of the hypercapnia of OHS patients. Some authors have proposed to not include SAS patients in the entity of OHS, because sleep apnea can sometimes induce hypercapnia per se, even in nonobese patients. However, we agree with most authors in not considering SAS as an exclusionary criterion for the diagnosis of OHS.2″ There is a subgroup of patients with SAS and OHS who have persistent nonapneic desaturation on polysomnography even after the elimination of occlusive apneas with nasal CPAP therapy. Despite a reduction in the resistive load against which the ventilatory pump must work by nasal CPAP therapy, hypoxemia and hypercapnia often persist during sleep and wakefulness in those patients. To avoid the confounding effect of hypoventilation as a consequence of SAS, we chose to include in this study only patients with severe respiratory failure because, in this subset of patients, it seems unlikely that upper airway obstruction could be the dominant mechanism of hypoventilation.
The role of NIPPV in the management of OHS is not well-established, particularly regarding its longterm use. The first successful trial for treating OHS involved the use of CPAP therapy in two patients with coexisting severe SAS. The success of this modality of treatment has been confirmed by other authors, although in studies with small numbers of patients. However, several articles have reported that CPAP therapy could not improve respiratory failure, at least initially, in some patients with OHS and SAS, while NIPPV therapy was effective in treating these patients. It has been found that NIPPV therapy can effectively unload the inspiratory muscles in severely obese patients with increased impedance of the respiratory system. The results of other studies- have suggested that NIPPV treatment improves the clinical symptoms and prevents respiratory failure in OHS patients to a degree similar to that reported for patients with diseases in which its use has been completely established (eg, kyphoscoliosis). It is time to start bridening your mind together with Canadian neighbor Pharmacy.
The present study describes, to our knowledge, the largest group of OHS patients to have been treated with NIPPV. Also, our report is the first systematic evaluation of the long-term evolution of these cases. Our results confirm that NIPPV therapy is useful in treating these patients with particularly severe OHS, both in the short term and after long periods of time. Noninvasive ventilation was found to be successful both when it was started in clinically stable patients and when it was implemented in those with respiratory acidosis. In this subgroup of patients, it has proved to be an effective alternative to intubation and ICU admission. Subjective symptoms (eg, dyspnea and daytime somnolence) and diurnal arterial blood gas values were improved by NIPPV therapy at night. Also, the therapy was useful in avoiding further hospital admissions because of respiratory exacerbations, except in five cases (9.2%). Only one of the deaths during the follow-up period was related to OHS (a 77-year-old woman with severe comorbidity, in which orotracheal intubation was not considered). Long-term NIPPV therapy was well-tolerated, but we must remark that 15 patients (21.7%) rejected the treatment after an initial trial. We have found large percentages of treatment rejection in women and patients with psychiatric disorders. The overall mortality rate (46%) was higher among untreated patients than among those who accepted treatment with NIPPV. Unfortunately, patients who refused to receive NIPPV treatment were lost to follow-up, and the cause of death could not be assessed in the majority of the patients.
We want to emphasize some practical aspects regarding the implementation of NIPPV therapy in our patients. Some of our patients did not totally correct their blood gases values during the hospital admission, and many maintained a certain level of hypercapnia on hospital discharge. We have found that PIP levels of > 20 cm H2O were usually poorly tolerated. The employed PIP levels were sometimes unable to lower the Pco2 values into the normal range in the short term. In fact, many patients initially required oxygen supplementation to maintain adequate oxygen saturation values (which to some degree also has been found by other au-thors’). However, by the first month of treatment, most patients had a resolution of the diurnal respiratory failure. None of the patients had attended the hospital or the emergency department during the first month of therapy. Therefore, it seems that it is not necessary to achieve a total correction of the diurnal blood gas values within the first weeks of treatment. As soon as the clinical condition of the patient remains stable and the pH is within normal values, the treatment will probably be effective. The use of bilevel pressure devices seems warranted, although achieving a total correction of the respiratory failure in the short term with these systems can be, in our experience, more difficult than with volume-cycled ventilators. Certainly, volume-cycled ventilation has the distinct advantage of being able to generate higher PIP values. However, the medium-term and long-term evolution of the patients with pressure-preset equipment seems adequate, and is no worse than other series in which patients were treated with volume-cycled devices. It must be noted that the number of patients in our series who could be treated initially with conventional CPAP therapy was low. However, a second sleep study performed once the patients became stabilized allowed that the conditions of more of them could be maintained with nasal CPAP therapy alone.
Some limitations of the present study, due to its retrospective design, must be addressed, the most important of which is the lack of a control group for the patients. Unfortunately, patients who did not accept or tolerate NIPPV treatment were lost to follow-up, making it impossible to compare their clinical evolution with that of the treatment group. In second place, compliance with NIPPV therapy was not formally assessed, but rather was based on the self-reports of patients. Therefore, the high levels of compliance with treatment found in our study might be somewhat overestimated. Finally, also due to the design of the study, we could not evaluate the time required for the patients to continue receiving NIPPV treatment before a trial to establish a CPAP regimen can be attempted. Piper and Sullivan have found that, in some cases, about 1 to 3 weeks of treatment is a sufficient period. However, other patients need as long as 3 months of NIPPV therapy before they can switch to CPAP treatment. In the opinion of Piper and Sullivan, if no clear improvement has occurred by this time, it is unlikely that CPAP can be a viable therapy. It must be remarked that even with a total reversal of the diurnal respiratory failure, it cannot be guaranteed that the patient’s condition will be controlled in the future by simple CPAP treatment. Most of our patients required the continuation of NIPPV therapy despite total stabilization. This was because CPAP treatment could not totally control the respiratory failure during the night, as assessed by polysomnography.
NIPPV could be withdrawn in only six of our patients, who had achieved enough weight loss. Although initially some patients lost weight under a dietetic program, most of them regained it quickly. This result is in agreement with observations made in other studies. Therefore, it is probable that most patients with OHS will need some kind of ventilatory support over the long term.
Several conclusions can be drawn from this study. In patients with decompensated hypercapnic respiratory failure due to OHS, NIPPV therapy results in a dramatic reversal of respiratory acidosis, avoiding orotracheal intubation. Normal or near-normal PaCO2 and PaO2 values were achieved 1 month after hospital discharge. When accepted by the patient, domiciliary NIPPV therapy was generally well-tolerated and was associated with excellent survival. Furthermore, NIPPV therapy provides a significant clinical improvement and maintains control of diurnal arterial blood gas tensions in the majority of OHS patients.