CHAPTER 6. DISCUSSION
6.1. Demographics and BO findings
experiencing sleepiness whilst driving. In the face of their severe subjective ratings of the other sleepiness questions, the latter is an interesting finding which raises the question of whether the participants were rather wary of reporting this question honestly, or that they over-reported other sleepiness questions. Empirical data suggests that subjects are reluctant to report sleepiness whilst driving for fear of restriction on driving or loss of driver's licence (Rosenthal, 2005). Subjectively, these patients reported symptoms and behaviour, which falls into a high-risk category.
A BMI >30kg/m2 and a history of high blood pressure were reported by 57% of the subjects. Many of these patients expressed "not knowing" whether they qualified for these symptoms or not, the findings could therefore have been over or under reported.
Nevertheless, if extrapolated to the general population in South Africa this figure suggests that just over half of a clinical population (in other words patients referred to specialist facilities for suspected OSA, or high-risk symptoms) could be suffering with an elevated BMI in the obese range and a history of high blood pressure. The impact on the
biopsychosocial and economic areas is profound, not only in terms of mental health but prescription medication as well.
6.2. HypnoPTT™ findings
From the final analysis of the HypnoPTT™ objective findings, the average heart was not used for analysis. The physician's result proved to be a reliable indicator of the severity ratings from the HypnoPTT™ data. The AHI showed an equal distribution of patients not experiencing breath-holding to those experiencing breath-holding within the mild and severe range. Only 11 patients fell within the moderate range. The AHI in line with
empirical data showed the most robust correlations with the physician's final report (r = .19, p < 0.01). ANA's were also significant markers of the final report outcomes (r = .76, p < 0.01). In addition the lowest oxygen saturation level was also significant (r = .71, p <
0.01). An AHI of >5 events per hour is considered abnormal in some countries, whist others start 10. Only 35 patients in this sample do not fall within the abnormal range, which suggests that most patients in this sample will suffer the consequences of OS A if not treated. Whilst the cohort of this study will benefit from treatment, those in lower socio-economic brackets may not, unless policy changes. According to the literature reviewed, the sort of risk factors we could expect particularly in the severe range of untreated patients, would be obesity, male gender, upper airway abnormalities, cardio- vascular (particularly hypertension) and pulmonary disease, genetic predisposition.
Symptoms such as headache, anxiety, depression, sexual dysfunction, cognitive
impairment, reduction of grey matter in the brain, frontal lobe deficits and performance degradation, may be the presenting problems. This daunting list provides the way forward for well-supported argument regarding the impact of these risk factors and symptoms on the individual, family, occupation and community. The cost to self and state will be enormous in the untreated patients. This could be extrapolated to the number of subjects who have not been identified. No epidemiology studies have been documented in South Africa to give us an indication of the extent of the problem.
Prolonged oximetry recordings shows that the lowest oxygen saturation level mean for the sample was 78% with a range of 49-97%. This effectively means that the majority of patients saturated as low as 85-90% and in 20 patients levels fell below 60%. According to Stevens (2004) all these levels are considered low for basic physiological function and the critically low and/or fluctuation of oxygen levels may suggest the presence of
Cheyne-Stokes (noted in the late stages of cardio-vascular disease) or periodic breathing.
This finding suggests that this sample of patients is at high risk for physiological deficits such as frequent autonomic arousals when the medulla is activated by fluctuating gaseous exchange (Somers, 2004). Furthermore sympathetic nervous system function is also alerted causing symptoms such as frequent urination. In addition, metabolic function is undermined (Ibid).
Excessive snoring and ANA's were recorded in most patients. The majority of patients experienced between 30-70 autonomic arousals during the sleep recording. This
extrapolates to extreme restlessness and sleep fragmentation. Stradling & Davies (2004) define sleep fragmentation as follows. The presence of snoring increased upper airway resistance and resultant rise in inspiratory effort, which in turn causes recurrent micro- arousals - even without evidence of apnoea, hypopnoeas or hypoxia (upper airway resistance syndrome). Apnoea increases resistance to the level of prolonged partial and full arousals from sleep. The pattern of breath-holding, inspiratory effort and awakening is cyclical and persistent throughout the night. Martin (1997) produced some evidence that one night of sleep fragmentation and 'autonomic arousals' can have small effects on daytime function. The ability to measure daytime function (apart from the ESS) is disappointing but is gaining momentum, however the measurement of performance in a sleepy individual clearly shows decrements after fragmented sleep or prolonged sleep debt. The sample studied in this research are clearly at risk in terms of the profound sleep fragmentation experienced and the subsequent consequences that may ensue. The
greatest concern lies with feeling sleepy whilst driving, which impacts on self and others.
Micro-sleeps and early onset sleep can lead to motor vehicle accidents (Brown, 1994;
Dinges, 1995; Harrison and Home, 1996; Thorpy, 2005). Productivity is also affected, impacting on the social and occupational aspect of the patient's life (Rosekind, 2005).