Obese patients with OSA have been observed to show significant severity than the nonobese OSA patients in terms of various parameters such as AHI, average as well as minimal oxygen saturation, arousal and desaturation indices.[20
] The present study has also shown similar findings and strikingly the minimal oxygen saturation was well below 90% in both the groups. The etiology of OSA in obese has been linked with anatomic alterations that predisposes to upper airway obstruction during sleep. Obesity seems to have two distinct mechanical influences on the pharyngeal airway collapsibility.[25
] First, it increases soft tissue surrounding the pharyngeal airway within limited maxillo-mandibular closure occupying and narrowing its space (pharyngeal anatomical imbalance). It can be considered that elevations in neck circumference and increased deposition of peripharyngeal fat could narrow and compress the upper airway.[26
] Furthermore, increased peripharyngeal fat has been correlated with increased sleep apnea severity.[28
] Second, it increases visceral fat volume that decreases lung volumes such as functional residual capacity (FRC) and expiratory reserve volume (ERV) leading to increased pharyngeal wall collapsibility possibly through decreased longitudinal tracheal retraction. Thus, obesity imposes mechanical loads on both the upper airway and respiratory system that predispose to upper airway narrowing, collapse, and airflow obstruction during sleep. Neural compensation for functioning structural abnormalities operating during wakefulness is also lost during sleep. These effects may be mediated by circulating adipokines, which influence body fat distribution and central nervous system activity.[30
In contrast, Sakakibara et al
. observed that the etiology of OSA in nonobese patients appears to be somewhat different which includes bony structure discrepancies.[17
] In accordance with this study, we observed shorter thyromental distance in the nonobese patients which signifies that the position of the chin is relatively low with reference to the thyroid cartilage and shorter length of the anterior cranial base.[31
] A retrospective study from Thailand also reported similar findings in 71 nonobese patients.[18
] Nonobese OSA patients tend to present the following anatomical craniofacial characteristics such as caudal hyoid, increased soft palate dimensions, and consequent anteroposterior reductions of the airways at the soft palate level, reduction of anteroposterior region of nasopharynx, and oral pharynx. Obese OSA patients can present with these findings but in addition they have increased volume of tongue and anterior hyoid bone. Lower and anterior position of hyoid bone in obese patients seems to be related to increased fat deposition on the tongue, which increases its volume.[32
] It has been suggested that the discrepancy in these cephalometric measurements may also depend on sex, age, and race.[33
] OSA in Asian men has been found more frequently in the nonobese patients, despite the presence of severe illness, when compared with white male patients with OSAS.[35
The present nonobese subjects were more likely in habit of taking sedatives for sleeping as compared to obese counterpart which is in concordance with study conducted by Ghanem and Mahmood on 102 patients with OSA.[21
] The incidence of hypertension was observed to be more in the obese OSA patients than the non-obese patients. This finding has been supported by several cross-sectional, longitudinal, and treatment studies.[38
] Obesity and OSA are each very strongly associated with hypertension.[43
] OSA is independently associated with hypertension, independent of obesity. Furthermore, obesity and OSA often co-exist and, in fact, one may be conducive to the other. It is therefore plausible that at least part of the association between obesity and hypertension is related to the presence of OSA and perhaps vice versa
. The presence of OSA in the obese patients may further contribute to adverse cardiovascular outcomes including hypertension when compared with each condition in isolation.[44
] OSA probably contributes to or exacerbates the obesity-related hypertension. OSA should be strongly suspected in obese individuals with resistant hypertension, those with the absence of a nocturnal decrease in blood pressure, those with unexplained weight gain or difficulty losing weight, and in those with symptoms suggestive of OSA. The diagnosis of OSA in this context is therefore of considerable clinical importance.
There are some potential limitations to this study. One limitation of the study was that we have considered parameters such asthyromental distance and Mallampati grading for cephalometric analysis as they are easy and cheap to perform in clinical practice and can correlate with severity of OSA. There are multiple imaging techniques to evaluate the upper airway in patients with OSA such as cephalometric radiography, CT, MRI, fluoroscopy, and somnofluoroscopy but these methods are cumbersome and expensive. Cephalometry is a diagnostic procedure to collect information on skeleton abnormalities and soft tissues of patients with OSA, providing support for indication of surgery. This should be based on disease severity and the presence of anatomical alterations of upper airway and of craniofacial skeleton. Another limitation is that the findings of this study need to be confirmed in a large number of samples.
It can be concluded that obstructive sleep apnea is not uncommon in the nonobese persons contrary to earlier concept that OSA is confined to the obese persons. Therefore, whenever a nonobese patient presents with a clinical picture suggestive of OSA, the diagnostic possibility should not be underestimated and should be evaluated thoroughly.