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Short-Term and Long-Term Effects of Nasal Intermittent Positive Pressure Ventilation in Patients With Obesity-Hypoventilation Syndrome*

Posted on: Tuesday, 23 August 2005, 03:00 CDT

Objective: To assess the outcome of 54 patients with obesity- hypoventilation syndrome (OHS) who were treated with nasal intermittent positive-pressure ventilation (NIPPV).

Design: Descriptive analysis of retrospectively collected clinical data.

Materials and methods: From March 1995 to December 2002, OHS (defined as a body mass index [BMI] of > 30 kg/m^sup 2^, a daytime PaCO^sub 2^ of ≥ 50 mm Hg, and a PaO^sub 2^ of < 60 mm Hg in the absence of COPD) was diagnosed in 69 cases. Fifteen patients (21.7%) refused to be treated with NIPPV, and 20 patients were started on NIPPV therapy electively and 34 following an acute exacerbation. We employed daytime arterial blood gas values and overnight pulse oximetry to determine the initial NIPPV modes and settings. The outcome measures were survival, clinical status, and arterial blood gas levels.

Results: Among the 54 study patients (18 women), the mean ( SD) age was 56 13 years. The mean BMI was 44 8.8 kg/m^sup 2^. Sleep apnea syndrome (apnea-hypopnea index, > 5) was present in 87% of the patients. At presentation, 22 of the 54 patients had experienced an acute hypercapnic respiratory failure (pH < 7.34). None of these patients required orotracheal intubation after NIPPV treatment. Initially, 2 patients were treated with volume-preset ventilation, 49 patients used pressure-preset equipment, and 3 patients employed continuous positive airway pressure (CPAP). Forty-seven patients required supplemental oxygen. At the end of the follow-up period (mean duration, 50 months), PaO^sub 2^ had increased by 24 mm Hg from baseline (95% confidence interval [CI], 21 to 28 mm Hg; p < 0.0001) and PaCO^sub 2^ had decreased by 17 mm Hg (95% CI, 13 to 20 mm Hg; p < 0.0001). NIPPV therapy improved subjective sleepiness (mean Epworth sleepiness scale score decrease, 16 5 to 6 2; p < 0.001), and dyspnea decreased in all but four patients. During follow-up, three patients died (one of them due to the progression of respiratory failure). NIPPV therapy could be withdrawn in 5 patients who had achieved a sufficient weight loss, and the conditions of 16 patients could be maintained without respiratory failure by the use of simple therapy with CPAP.

Conclusions: NIPPV therapy is effective in the treatment of patients with OHS, providing a significant improvement in clinical status and gas exchange. (CHEST 2005; 128:587-594)

Key words: hypercapnic respiratory failure; noninvasive mechanical ventilation; obesity hypoventilation syndrome; piclcwickian syndrome; sleep apnea

Abbreviations: AHI = apnea-hypopnea index; BMI = body mass index; CI = confidence interval; CPAP = continuons positive airway pressure; ESS = Epworth sleepiness scale; NIPPV = nasal intermittent positive pressure ventilation; OHS = obesity-hypoventilation syndrome; PEP = positive expiratory pressure; PIP = positive inspiratory pressure; SaO^sub 2^ = arterial oxygen saturation; SAS = sleep apnea syndrome; TLC = total lung capacity

The incidence of obesity, defined as a body mass index (BMI) of > 30 kg/m^sup 2^, is increasing dramatically in Western society. As obesity progresses, hypoventilation may develop in some individuals, leading to respiratory failure and premature death.1 Obesity- hypoventilation syndrome (OHS) is a clinical entity that is characterized by the coexistence of obesity and hypercapnia during wakefulness.2 Patients with OHS are heavy users of health-care resources prior to receiving treatment of their disorder.3 Noninvasive positive-pressure ventilation (NIPPV) has been successfully used in treating patients with other diseases, such as kyphoscoliosis, neuromuscular diseases, and central hypoventilatory disorders, in which the patient presents with hypercapnia. However, there is little information on the impact of NIPPV therapy on survival and functional status in individuals with OHS, and data regarding the long-term evolution of the patients are particularly scarce. We report herein our experience with NIPPV as both a short- term and a long-term intervention in the treatment of 54 patients with OHS.

FIGURE 1. Enrollment and treatment of patients. AURF = acute hypercapnic respiratory failure (ie, patients with a pH of < 7.34 at hospital admission); CRF = chronic respiratory failure (ie, patients with a pH of ≥ 7.34 at hospital admission).

MATERIALS AND METHODS

Patients

From March 1095 to December 2002, OHS was diagnosed in 69 patients. These patients met the following criteria: (1) obesity with a BMI of >30 kg/m^sup 2^; (2) hypercapnic respiratory failure at the moment of diagnosis (PaCO^sub 2^, ≥ 50; PaO^sub 2^, < 60 mm Hg); (3) FEV^sub 1^/FVC ratio of ≥ 70%; (4) the absence of any respiratory disorder that could be responsible for the gas- exchange impairment (eg, kyphoscoliosis and diaphragmatic paralysis); and (5) a iollow-up period of > 12 months. Fifteen patients (21.7%) rejected the treatment with domiciliary NIPPV. Unfortunately, these patients were not followed up, but we reviewed their charts and telephoned them or their families to inquire about their current medical condition. The remaining 54 patients received NIPPV therapy for a minimum of 1 year. NIPPV therapy was started electively in 20 patients and following an episode of acute respiratory failure in the remaining 34 patients (Fig 1). All of them were treated in a conventional respiratory medical ward, where physicians and nurses were trained in NIPPV techniques. Data were collected by reviewing the records of the Hospital Xeral-Calde using a standardized form.

NIPPV Technique and Monitoring

Treatment with NIPPV was started in all patients who experienced respiratory failure presumed to be secondary to OHS. Patients were treated initially with bilevel pressure devices (DP-90 and Eclipse Delta; Taema; Antony, France; and PV-102^sup +^; BREAS; Gothenburg, Sweden), but, in those patients who did not achieve sufficient improvement with this system, we subsequently changed over to a volume-cycled ventilator (Home 2; Airox; Pau, France). The interface used in all patients was a commercially available nasal mask that was secured with head straps. Initially, positive expiratory pressure (PEP) was set at 6 cm H2O, and the positive inspiratory pressure (PIP) was set at 10 cm H2O. PIP was gradually adjusted upward as tolerated. Oxygen was administered, when needed, through the mask until the arterial oxygen saturation (SaO^sub 2^) was ≥ 90%. Daytime sessions lasted from 3 to 6 h with pauses of 3 h to allow the administration of conventional medication and feeding. Nighttime sessions were continuous, provided that patient tolerance permitted. When arterial blood gas levels were stable (ie, pH > 7.35), daytime NIPPV therapy was stopped. We employed daytime arterial blood gas measurements and overnight pulse oximetry to determine the NIPPV settings. We gradually increased PEP until the disappearance of repetitive dips in SaO^sub 2^ was achieved. PIP was then increased until an acceptable level of steady saturation was obtained. We considered treatment with NIPPV to be successful if orotracheal intubation had been avoided in patients with an initial pH of < 7.34 and, for the entire group, when the mean SaO^sub 2^ during overnight oximetry was ≥ 88% and diurnal PaCO^sub 2^ was ≥ 65 mm Hg with a normal pH. Then, the patients could be discharged from the hospital, and they were instructed to employ NIPPV during the night with the final settings obtained.

Measurements

Daytime sleepiness was evaluated according to an Epworth sleepiness scale (ESS) questionnaire. A change in any lower degree of the scale was considered as an improvement in sleepiness. Dyspnea was evaluated using the modified Medical Research Council dyspnea scale. We performed conventional spirometry with a 10-L, closed- circuit spirograph. Static lung volumes were measured by the helium dilution method (GS; Collins; Braintree, MA). The predicted values used were those of the European Respiratory Society.4 We measured arterial blood gas levels while the patients were awake, sitting, and breathing room air. Nocturnal oximetric data were computed from night oximetry (Vitalog VX4 pulse oximeter; Respironics; Murrysville, PA) that was performed separately from polysomnography. Polysomnography was performed once the patients were discharged from the hospital, and they had achieved a stable clinical condition. For staging sleep we recorded an EEG (C4A1 and O3A2), a chin electromyogram, and an electrooculogram. Thoracoabdominal excursions and oronasal airflow were measured qualitatively. Arterial oxyhemoglobin saturation was recorded using a finger oximeter. These variables were recorded on a multichannel polygraph (Alice 3; Healthdyne; Marietta, GA). Sleep apnea syndrome (SAS) was defined as apnea-hypopnea index (AHI) of > 5.

Follow-up

All patients underwent a medically supervised and intensified dietary regimen. In selected patients, a weight-reduction surgical intervention was performed. During follow-up, clinical evaluation, repeat pulmonary function testing, and arterial blood gas measurements were performed. Compliance with NIPPV therapy was not formally measured, but rather it was assessed according to patients' self-reports. During a second \sleep study night, the final NIPPV settings were determined. We first employed nasal continuous positive airway pressure (CPAP) in eveiy patient. The CPAP was adjusted with the aim of preventing apneas and hypopneas in all sleep stages. Oxygen was added it required. When significant oxygen desaturation persisted despite the use of high pressures, CPAP was considered to have failed, and we subsequently changed over to a pressure or volume ventilator.

Statistical Analysis

All data were expressed as the mean SD. The effectiveness of therapy was assessed by comparing the follow-up awake PaCO^sub 2^ and PaO^sub 2^ values to the corresponding values prior to the initiation of NIPPV therapy. For this analysis, paired group comparisons were performed using a f test for two groups and the Friedman test for more than two groups. A value of p < 0.05 was considered to he statistically significant. Descriptive statistics were done by using a statistical software package (SPSS, version 10.0 for Windows; SPSS, Inc; Chicago, IL).

RESULTS

Characteristics of the Patients

Fifteen patients (10 female and 5 male; mean age, 62 years) did not accept NIPPV therapy after an initial trial. When comparing patients who opted for home NIPPV therapy and those who did not, no significant difference was noted in terms of age, weight, BMI, and baseline gasometric values. However, there were more women (67% vs 33%, respectively; p = 0.04) and higher rates of psychiatric disorders (60% vs 18%, respectively; p = 0.004) in the group of patients who refused NIPPV therapy. Seven patients (46%) in this group died during the period of the study (Fig 1).

Among the 54 study patients, the mean age was 56 13 years; 18 patients (33.3%) were women. The mean BMI was 44 9 kg/m^sup 2^, indicating severe obesity. Approximately 77% of the patients had comorbid diseases. Ten patients (18.5%) had a history of physician- diagnosed asthma. All but three patients claimed to have dyspnea on exertion. Forty-seven patients complained of excessive daytime sleepiness (mean ESS score, 16 5), and 36 patients exhibited peripheral edema. Seven patients (13%) were found to be free of SAS. The remaining 47 patients had SAS with a mean AHI of 43.3 25.6. The baseline characteristics of the study population are shown in Table 1.

Pulmonary Function

Lung Volumes and Flows: The mean FVC was decreased at 60% of predicted. Forty-four patients demonstrated a reduced FVC (< 80%), mostly due to a reduction in expiratory reserve volume that was compatible with obesity. The average FEV^sub 1^/FVC ratio was 83%. The mean total lung capacity (TLC) was 87 13% of the predicted value, and 12 patients showed a restrictive pattern (TLC, < 80% predicted). These results are shown in Table 2.

Table 1-Patient Characteristics*

Gas Exchange: At baseline, all patients were hypercapnic with a mean PaCO^sub 2^ of 60 10 mm Hg. The mean PaO^sub 2^ was 46 9 mm Hg, and the mean pH was 7.34 0.17 (Table 2). Thirty-four patients were treated following an acute exacerbation. In this group of patients, the mean pH was 7.33 (range, 7.17 to 7.45).

Table 2-Pulmonary Function*

Pulse Oximetry: At baseline, an overnight pulse oximetry could be performed in 41 patients. The mean sleep SaO^sub 2^ was 79 5%, the mean time spent at an SaO^sub 2^ < 90% was 85 19%, and the mean oxyhemoglobin nadir during sleep was 46 11% (Table 2). Patients with more severe gas exchange impairment that required rapid NIPPV intervention could not be assessed.

In-Hospital NIPPV Treatment and Outcome: At presentation, 22 of the 54 patients had experienced an acute hypercapnic respiratory failure (pH, < 7.34). None of these patients required orotracheal intubation. In this subgroup of acidotic patients, gasometric values were available for 15 of them after 24 h of treatment with NIPPV; PaO^sub 2^ increased by 4 mm Hg from baseline (95% confidence interval [CI], 0.8 to 9 mm Hg; p = 0.09), PaCO^sub 2^ decreased by 7 mm Hg (95% CI, 2 to 12 mm Hg; p = 0.009), and pH increased by 0.07 (95% CI, 0.02 to 0.08; p = 0.01). Considering the whole group of OHS patients, PaO^sub 2^ had increased by 12 mm Hg at hospital discharge (95% CI, 9 to 14 mm Hg; p < 0.0001), and PaCO^sub 2^ fell by 12 mm Hg (95% CI, 9 to 15mm Hg; p < 0.0001) compared to pretreatment values. The in-hospital gas exchange evolution is shown in Table 3. The mean length of hospital stay was 8.4 4 days. At hospital discharge, the most frequent NIPPV modality employed was bilevel positive-pressure ventilation. The PIP levels ranged from 12 to 30 cm H2O (mean, 18 3 cm H2O), and the PEP levels ranged from 5 to 13 cm H2O (mean, 9 2 cm H2O). Volume-cycled ventilation and CPAP were used to a much lesser extent. The NIPPV modes used at hospital discharge are shown in Table 4.

Late Follow-up: The mean follow-up period was 50 25 months (range, 12 to 105 months). Dyspnea improved in all but four patients. The mean ESS score changed from 16 5 at baseline to 6 2 after follow-up (p < 0.05). The comparison of pretreatment with the last posttreatment measurements demonstrated significant improvements in both mean PaO^sub 2^ values (70 9 mm Hg; p < 0.0001 [Friedman test]) and mean PaCO^sub 2^ values (44 7 mm Hg; p < 0.0001 [Friedman test]). PaO^sub 2^ increased by 24 mm Hg (95% CI, 21 to 28 mm Hg), and the PaCO^sub 2^ decreased by 17 mm Hg (95% CI, 13 to 20 mm Hg). Only five patients (9%) failed to maintain a PaO^sub 2^ of > 55 mm Hg and a PaCO^sub 2^ < 50 mm Hg, but three of those patients could lower the PaCO^sub 2^ into the normal range with additional changes in the ventilation modes or settings. These patients were no different in terms of age, weight, AHI, or gasometric values. Figure 2 shows the changes in arterial blood gas tensions during follow-up. A comparison of pulmonary function tests before and after NIPPV demonstrated no significant improvement in FVC (62 17% predicted), TLC (88 8% predicted), and residual volume (134 32% predicted).

Table 3-In-Hospital Gas Exchange Evolution*

Nineteen patients (35.1%) were admitted to the hospital during follow-up (5 of them due to respiratory failure). Three patients died during this period, but death was attributed to OHS in only one case. No significant weight loss was observed at the end of follow- up period (p = 0.95 [Friedman test]). The mean BMI at the final evaluation was 40 8 kg/m^sup 2^. However, five patients who achieved a significant weight reduction were able to wean from NIPPV. Two patients underwent weight reduction surgery; and both of them lost a significant amount of weight and no longer required NIPPV therapy. Five patients reported "irregular" or "less than optimal" compliance with NIPPV therapy.

Thirty-one patients (57.4%) underwent a second polysomnography. NIPPV tritration allowed that more patients could be maintained out of respiratory failure by the use of simple CPAP therapy. The NIPPV modes used after follow-up are shown in Table 4.

DISCUSSION

Obesity can have detrimental effects on respiratory function,5 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.6,7 Some available data support a possible role for airway obstruction in the pathogenesis of diurnal hypercapnia in certain patients with OHS and SAS,8,9 although this finding has not been confirmed in other studies.10,11 We think that most authors would exclude patients with significant COPD from the diagnosis of OHS,12,13 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 authors12 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.9 However, we agree with most authors in not considering SAS as an exclusionary criterion for the diagnosis of OHS.2,13 There is a subgroup of patients with SAS and OHS who have persistent nonapneic desaturation on polysoirmography 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.14 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 hvpoventilation.

Table 4-NIPPV Modes at Hospital Discharge and After Follow-up*

The role of NIPPV in the management of OHS is not well- established, particularly regarding its long-term use. The first successful trial for treating OHS involved the use of CPAP therapy in two patients with coexisting severe SAS.15 The success of this modality of treatment has been confirmed by other authors,16 although in studies with small numbers of patients. However, several articles17-19 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.20 The results of other studies21,22 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).

FIGURE 2. Changes in arterial blood gas tensions during the follow-up period.

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 PCO^sub 2^ 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 authors21,22). 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 series22 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 Sullivan19 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,19, 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.23 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 PaCO^sub 2^ and PaO^sub 2^ 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.

* From the Respiratory Division (Drs. Prez de Llano, Ortiz Piquer, and Veres Racamonde) and the Sleep Disorders Laboratory (Drs. Vzquez Caruncho, Ms. Caballero Muinelos, and Ms. Alvarez Carro), Hospital Xeral-Calde, Lugo, Spain; and the Respiratory Division (Dr. Golpe), Hospital Monforte, Lugo, Spain.

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Luis A. Prez de Llano, MD; Rafael Golpe, MD; Montserrat Ortiz Piquer, MD; Alejandro Veres Racamonde, MD; Manuel Vzquez Caruncho, MD; Olga Caballero Muinelos, RN; and Cristina Alvarez Carro, RN

Manuscript received August 3, 2004; revision accepted February 16, 2005.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml).

Correspondence to: Luis A. Prez de Llano, MD, Respiratory Division, Hospital Xeral-Calde, c/Dr. Ochoa s/n, 27004 Lugo, Spain; e-mail: luis@ciberque.com

Copyright American College of Chest Physicians Aug 2005

Source: Chest

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