Cystic echinococcosis: late rupture and complication of a stable pulmonary cyst.

Cystic echinococcosis is observed worldwide. Traditional management includes an invasive surgical approach with adjunctive chemotherapy. It has been suggested that observation alone may be appropriate in asymptomatic individuals with stable cysts. A case involving a 38-year-old Peruvian man with an asymptomatic bronchogenic cyst (suspected to be due to echinococcus, but never definitely diagnosed) is presented. The cyst was first noted in 1998, and was followed for 10 years during which time he remained asymptomatic with minimal radiographic change. One year later, in 2009, he presented with acute rupture of the cyst causing empyema. The patient required thoracotomy, decortication and resection of the ruptured cyst. Final pathology showed Echinococcus organisms. The patient responded well to treatment with albendazole and praziquantel, and became completely asymptomatic within six months. The present case demonstrates that echinococcal cysts may be at risk of spontaneous rupture, even after many years of clinical stability, thus supporting the case for resection of asymptomatic cysts suspected of being echinococcal at the time of diagnosis. In addition, the case illustrates that medical therapy with albendazole and praziquantel, in conjunction with surgical drainage, can be successful in the treatment of echinococcal empyema.

Pharyngeal narrowing in end-stage renal disease: implications for obstructive sleep apnoea.

Sleep apnoea is common in patients with end-stage renal disease (ESRD). It was hypothesised that this is related to a narrower upper airway. Upper airway dimensions in patients with and without ESRD and sleep apnoea were compared, in order to determine whether upper airway changes associated with ESRD could contribute to the development of sleep apnoea. An acoustic reflection technique was used to estimate pharyngeal cross-sectional area. Sleep apnoea was assessed by overnight polysomnography. A total of 44 patients with ESRD receiving conventional haemodialysis and 41 subjects with normal renal function were studied. ESRD and control groups were further categorised by the presence or absence of sleep apnoea (apnoea/hypopnoea index > or =10 events.h(-1)). The pharyngeal area was smaller in patients with ESRD compared with subjects with normal renal function: 3.04 +/- 0.84 versus 3.46 +/- 0.80 cm(2) for the functional residual capacity and 1.99 +/- 0.51 versus 2.14 +/- 0.58 cm(2) for the residual volume. The pharynx is narrower in patients with ESRD than in subjects with normal renal function. In conclusion, since a narrower upper airway predisposes to upper airway occlusion during sleep, it is suggested that this factor contributes to the pathogenesis of sleep apnoea in dialysis-dependent patients.

Apnea and snoring: state of the art and future directions.

This review is intended to discuss the newer aspects of sleep apnea, and particularly where the new advances are likely to take place in the current millennium. The topics reviewed include epidemiology and clinical features of sleep apnea and snoring, adverse health consequences of sleep-disordered breathing, upper airway resistance syndrome, and treatment. Most of the work reviewed in these areas has been published since the year 2000, although whenever necessary older literature on the topic under discussion is summarized. Based on the accumulated information to date, new advances in the sleep-disordered breathing are likely to occur in the genetics of sleep apnea, identification of cellular mechanisms involved in control of vascular resistance, and pharmacological treatment of sleep apnea directed toward specific target such as pharyngeal muscles.

Comparing pressures required to abolish snoring and sleep apnea.

OBJECTIVE: Snoring and obstructive sleep apnea share similar pathogenesis and similar response to treatment with continuous positive airway pressure (CPAP). The purpose of this study was to compare pressures required to abolish apneas (POSA) with pressures required to abolish snoring (PSNOR). DESIGN: Cross-sectional, nonrandomized cohort study. SETTING: Sleep disorders clinic at St Michael's Hospital - a tertiary referral centre and a teaching hospital of the University of Toronto, Toronto, Ontario. POPULATION STUDIED: Unselected consecutive 441 patients with confirmed sleep apnea who were undergoing a CPAP titration study in the sleep laboratory. INTERVENTIONS: Nocturnal polysomnography using CPAP titration protocol, which required incremental increases in pressure until snoring and apnea were abolished or a maximum pressure of 16 cm H2O was attained. PSNOR and POSA were recorded and compared. RESULTS: Mean (+/- SD) pressures required to abolish snoring and apnea were: PSNOR 8.3+/-2.57 cm H2O and POSA 7.9+/-2.72 cm H2O (P<0.0001). In 75% of patients, the PSNOR was within +/-1 cm H2O of the POSA; in 92%, it was within +/-2 cm H2O; and in 97%, it was within +/-3 cm H2O. CONCLUSIONS: Empirically increasing pressure by 2 cm H2O in patients on CPAP who continue to snore may abolish snoring and apnea without the necessity of another titration study.

Obstructive sleep apnea and hypertension: from correlative to causative relationship.

Sleep-disordered breathing, manifested by repetitive episodes of partial or complete cessation of breathing during sleep associated with brief arousal and autonomic activation, is estimated to affect as many as 4% of adult men and 2% of adult women. Studies conducted during the 1980s revealed a strong association between sleep-disordered breathing and hypertension. The results of these early studies, which relied on relatively small samples of patients, have been confirmed in recent years by large-scale epidemiologic studies that are controlled for all possible confounding factors. This paper reviews the evidence suggesting a causative relationship between hypertension and disordered breathing in sleep. The authors discuss the possible underlying mechanisms of the two entities and address the clinical implications of this relationship. They conclude by recommending a proactive approach to the diagnosis of breathing disorders in sleep, in order to prevent the cardiovascular sequelae of this syndrome.

Sleep apnea syndrome: a possible contributing factor to resistant.

STUDY OBJECTIVES: There is evidence supporting an association between sleep apnea and hypertension. However, it is not clear if sleep apnea interteres with the pharmacotherapy of hypertension. To investigate this question, we studied the relationship between the effectiveness of anti-hypertensive treatment in reducing blood pressure, and severity of sleep apnea in a large group of apneic patients referred to a sleep disorders centre at St. Michael's Hospital at the University of Toronto. DESIGN: N/A. SETTING: N/A. PARTICIPANTS: 1,485 adult patients with sleep apnea, as defined by the apnea/hypopnea index (AHI) >10 events/hr, were analyzed. There were 393 who reported using anti-hypertensive medications on a regular basis for more than 6 months. One hundred and eighty-three patients were treated "effectively" (i.e. blood pressure lower than 140/90 mm Hg in the morning and in the evening). Seventy-four patients were treated "ineffectively," defined as blood pressure >140/90 mm Hg in the morning or in the evening. Both groups were compared with respect to clinical and demographic data using analysis of covariance with gender, age, body mass index (BMI), and neck circumference (NC) as covariates. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Ineffectively and effectively treated patients were similar in age (57 +/- 9) vs. 57 +/- 10 years, respectively), and had similar body mass index (33.8 +/- 7.4 vs. 33.4 +/- 7.3 kg/m2, respectively). However, ineffectively treated patients had significantly higher apnea/hypopnea index (44 +/- 29 vs. 33 +/- 25 events/hr, p<.0005), despite having similar nocturnal oxygenation (percent of total sleep time spent with oxygen desaturation lower than 90% was 36 +/- 34 vs. 29 +/- 30% in the ineffective and effective groups, respectively). The difference in AHI persisted even after adjusting for age, gender, and body mass index. CONCLUSIONS: Our results demonstrate that hypertensive patients with sleep apnea whose blood pressure responds beneficially to treatment have less severe sleep apnea than those patients whose blood pressure remains elevated despite anti-hypertensive therapy. Since neither obesity nor nocturnal hypoxemia appear to be important determinants of ineffective treatment, we suggest that resistant hypertension may be caused by frequent intermittent sympathetic stimulation.

Impact of menopause on the prevalence and severity of sleep apnea.

STUDY OBJECTIVES: To compare the prevalence and severity of sleep apnea between premenopausal and postmenopausal women, and to determine whether these differences are affected by the body mass index (BMI) and neck circumference. DESIGN: Cross-sectional study utilizing a sleep clinic patient database. SETTING: University hospital. PATIENTS: A total of 1,315 women, classified into premenopausal and postmenopausal groups based on age (< 45 years and > 55 years, respectively). MEASUREMENTS: Anthropometric measurements included height, weight, and neck circumference. Sleep measurements included full nocturnal polysomnography. Sleep apnea was defined as an apnea-hypopnea index (AHI) > 10/h. RESULTS: There were 797 premenopausal and 518 postmenopausal women. The latter group was more obese (mean +/- SE BMI, 32.2 +/- 0.4 kg/m(2) vs 30.2 +/- 0.4 kg/m(2); p < 0.0001) and had larger neck circumference (37.1 +/- 0.2 cm vs 35.8 +/- 0.2 cm; p < 0.0001). The prevalence of sleep apnea was greater in postmenopausal women than premenopausal women (47% vs 21%; chi(2) < 0.0001). There were proportionately more postmenopausal than premenopausal women in all ranges of apnea severity (AHI, 10 to 30/h, 30 to 50/h, and > 50/h). Postmenopausal women had a significantly higher mean AHI compared to premenopausal women (17.0 +/- 0.9/h vs 8.7 +/- 0.6/h; p < 0.0001); this significant difference persisted even after adjusting for BMI and neck circumference. CONCLUSION: There may be functional, rather than anatomic, differences in the upper airway between premenopausal and postmenopausal women, which may account for the observed differences in apnea prevalence and severity.

Upper airway pressures in snorers and nonsnorers during wakefulness and sleep.

OBJECTIVE: To compare upper airway pressures in snorers and nonsnorers during sleep and wakefulness. DESIGN: Case series of snorers and nonsnoring controls. SETTING: Sleep clinic of a university hospital. METHODS: We used open catheters to measure differential nasopharyngeal and hypopharyngeal pressures in 8 nonapneic snorers with excessive daytime tiredness and 10 healthy nonsnoring controls. Measurements were performed during sleep (with the mouth taped to ensure exclusively nasal breathing) and wakefulness. When awake, the subjects were either seated (with the head neutral, flexed, extended, or rotated) or recumbent (dorsal and lateral positions). MAIN OUTCOME MEASURES: Comparison of pressures within the group as a function of body position and between the groups as a function of snoring. RESULTS: Differential nasal and pharyngeal pressures were similar in seated snorers and nonsnorers independently of head position. Assumption of recumbency resulted in significantly increased pharyngeal pressures in nonsnorers (26 +/- 18 Pa seated vs. 52 +/- 46 Pa recumbent, p < .05) and snorers (50 +/- 35 Pa seated vs. 93 +/- 38 recumbent, p < .01). The increase was higher in snorers than nonsnorers. During snoring, sleep differential pharyngeal pressures in snorers were markedly increased compared to quiet sleep (567 +/- 450 Pa during snoring epochs vs. 117 +/- 82 Pa during nonsnoring epochs, p < .01). CONCLUSIONS: Compared to nonsnorers, recumbent nonapneic snorers have elevated differential pharyngeal pressures indicative of increased upper airway resistance and reduced airway patency; this is present during wakefulness and sleep.

Predicting effective continuous positive airway pressure.

PURPOSE: The purpose of this study was to compare the pressure required to abolish apneas as predicted from a previously derived algorithm (Ppred) with the true effective pressure (Peff) determined during a continuous positive airway pressure (CPAP) titration study. SETTING: Sleep clinic of a university hospital. METHODS: We prospectively studied 329 patients with sleep apnea undergoing CPAP titration. The following protocol was employed. Titration began at a pressure (Ppred) calculated from a previously derived equation based on body mass index, neck circumference, and apnea/hypopnea index (AHI). If AHI at Ppred was > 10, the pressure was increased in steps of 1 cm H(2)O until AHI became < 10. If, on the other hand, AHI at Ppred was < 10, the pressure was reduced in increments of 1 cm H(2)O until AHI became > 10. The lowest pressure that abolishes sleep apnea is defined as the Peff. Paired t tests, linear correlation, and distribution of (Ppred - Peff) were used to compare Peff and Ppred. RESULTS: Successful titration was accomplished in 276 patients (84%). Mean Ppred was similar to mean Peff (8.1 +/- 2.2 vs 8.1 +/- 2.6 cm H(2)O, respectively). There was a significant correlation between these two pressures (r = 0.73; p = 0.0001). Examination of the distribution of (Peff - Ppred) revealed that in 63% of patients, Ppred was within +/- 1 cm H(2)O of Peff; in 83% of patients, the two measures were within +/- 2 cm H(2)O; and in 95%, within +/- 3 cm H(2)O. CONCLUSION: We conclude that pressure predicted from an algorithm based on simple anthropometric and sleep variables constitutes a good starting point for CPAP titration, allowing the optimum pressure to be achieved with only a few incremental changes.

Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study.

OBJECTIVE: To assess whether sleep apnoea syndrome is an independent risk factor for hypertension. DESIGN: Population study. SETTING: Sleep clinic in Toronto. PARTICIPANTS: 2,677 adults, aged 20-85 years, referred to the sleep clinic with suspected sleep apnoea syndrome. OUTCOME MEASURES: Medical history, demographic data, morning and evening blood pressure, and whole night polysomnography. RESULTS: Blood pressure and number of patients with hypertension increased linearly with severity of sleep apnoea, as shown by the apnoea-hypopnoea index. Multiple regression analysis of blood pressure levels of all patients not taking antihypertensives showed that apnoea was a significant predictor of both systolic and diastolic blood pressure after adjustment for age, body mass index, and sex. Multiple logistic regression showed that each additional apnoeic event per hour of sleep increased the odds of hypertension by about 1%, whereas each 10% decrease in nocturnal oxygen saturation increased the odds by 13%. CONCLUSION: Sleep apnoea syndrome is profoundly associated with hypertension independent of all relevant risk factors.

Evaluation of variable mandibular advancement appliance for treatment of snoring and sleep apnea.

OBJECTIVE: To evaluate an adjustable mandibular positioning appliance for treatment of snoring and sleep apnea. METHODS: One hundred thirty-four patients with baseline apnea/hypopnea index (AHI) of 37 +/- 28 events/h (mean +/- SD) received the appliance. The efficacy of the appliance was assessed by the following investigations, performed at baseline and with the appliance: polysomnography, Epworth sleepiness scale, bedpartners' assessment of snoring severity, patients' assessment of side effects, and overall satisfaction. RESULTS: Thirteen patients were lost to follow-up. An additional 46 patients had no follow-up polysomnography, but answered the questionnaires. A total of 75 patients had polysomnography at baseline and with the appliance. We found a significant reduction in AHI from 44 +/- 28 events/h to 12 +/- 15 events/h (p < 0.0005) and a reduction in the arousal index from 37 +/- 27 events/h to 16 +/- 13 events/h (p < 0.05). Epworth scores fell from 11 +/- 5 to 7 +/- 3 (p < 0.0005). Bedpartners' assessment revealed marked improvement in snoring. For example, at baseline 96% of patients were judged to snore loudly "often" or "always" by their bedpartners, whereas only 2% were judged so while using dental appliance. The most frequent side effect was teeth discomfort, present "sometimes" or "often" in up to 32% of patients. Follow-up clinical assessment in 121 patients conducted on the average 350 days after the insertion of the appliance revealed that 86% of patients continued to use the appliance nightly; 60% were very satisfied with the appliance, 27% were moderately satisfied, 11% were moderately dissatisfied, and 2% were very dissatisfied. CONCLUSION: We conclude that the adjustable mandibular positioning appliance is an effective treatment alternative for some patients with snoring and sleep apnea.

Does nasal nitric oxide come from the sinuses?

OBJECTIVE: The purpose of this study was to assess nitric oxide (NO) output by the nose and sinuses. METHOD: In one volunteer, the osteomeatal complex and sphenoethmoidal recess were occluded to isolate the nose from the sinuses. The antrum and frontal sinus were each punctured by two catheters and irrigated with air at constant flow. Nitric oxide output and its rate of accumulation in the absence of air flow were measured in each sinus and in the adjacent nasal cavity. RESULTS: Prior to ostial occlusion, NO output in the nose was 96 nL/min. It decreased by 12% after blockage of all of the ostia. In the isolated sinuses, it was 190 nL/min (antrum) and 68 nL/min (frontal). After 5 minutes stagnation; NO concentration [NO] rose in the occluded sinuses to 24,700 nL/L in the antrum and 22,300 nL/L in the frontal sinus. In the nose, it increased to 29,000 nL/L. When the period of stagnation was prolonged in the frontal sinus, the [NO] reached a plateau. NO output and accumulation were not altered in the nose or either sinus by opening their ostia. In the antrum and frontal sinus, lidocaine reduced NO output and the rate of NO accumulation, but not in the nose. CONCLUSIONS: In this volunteer, 88% of nasal NO was derived from the nose itself. Nitric oxide exchange between the frontal sinus, antrum, and nose was negligible. In the absence of air flow, [NO] rose to a plateau in the nose and frontal sinus. Lidocaine inhibited NO output in the sinuses but not the nose.

Does snoring contribute to presbycusis?

It is well known that hearing acuity decreases with age. The precise mechanism responsible for this phenomenon, called presbycusis, is unknown. One hypothesis advanced to explain this loss of acuity implicates chronic exposure to snoring noise. Consequently, the purpose of this study was to investigate whether snoring is associated with hearing loss. We examined 219 patients (63 women and 156 men) referred to our sleep disorders center. All of the patients underwent nocturnal polysomnography with measurements of snoring, as well as standard audiometry (i.e., measurement of hearing thresholds at 250 Hz, 500 Hz, 1 kHz, 2 kHz, 3 kHz, 4 kHz, 6 kHz, and 8 kHz). Snoring was quantified by measuring three parameters: snoring index (SI = number of snores/h of sleep), average nocturnal sound intensity (dBav), and maximum nocturnal sound intensity (dBmax). We used simple correlation analysis to investigate the relationship between snoring and hearing thresholds; multiple linear regression analysis to determine individual contributions of age, sex, and snoring to the variability in hearing thresholds; and comparison tests to determine whether mild snorers had less hearing impairment than severe snorers. None of these statistical tests demonstrated that snoring was a significant determinant of hearing. We conclude that snoring is not associated with hearing loss and is therefore unlikely to account for presbycusis.

Is atelectasis following aortocoronary bypass related to temperature?

OBJECTIVE: To determine the frequency of acute postoperative atelectasis in patients undergoing aortocoronary bypass with either normothermic (warm) or hypothermic (cold) technique. DESIGN: Prospective, randomized study comparing two groups. SETTING: University-affiliated hospital. PATIENTS: Three hundred thirty-one patients (166 cold and 165 warm) undergoing isolated aortocoronary bypass. MEASUREMENTS: Chest radiographs were obtained preoperatively, on the day of surgery, and subsequently as clinically indicated until discharge from the hospital. Radiologist (blinded to the patient allocation into warm or cold group) scored the atelectasis from 0 to 3 based on its severity. Regression analysis was used to determine if there was any difference in the atelectasis scores between the two groups. RESULTS: Mean daily postoperative atelectasis scores were not different between the cold and warm groups. The number of patients requiring chest radiographs was similar in both groups. The percent of patients with abnormal chest radiographs was similar in both groups. CONCLUSION: The temperature of cardioplegia has no effect on the development of atelectasis following aortocoronary bypass, and therefore temperature-related cold injury is not a major cause of atelectasis following this type of surgery.

Comparison of direct and indirect measurements of respiratory airflow: implications for hypopneas.

The purpose of this study was to compare indirect methods for measuring respiratory airflow, such as temperature difference between inspired and expired air, thoracoabdominal movements, and nasal respiratory-airflow pressures-with a more direct measurement of minute ventilation using a head-out body plethysmograph. Measurements were obtained in healthy, awake, seated subjects during sequences of different levels of voluntary hypoventilations at 20 breaths/minute and analyzed to determine how well different methods could identify hypopneas (defined as reduction in minute ventilation by 50% or more). The results varied widely between different methods. Sensitivities ranged from 0 to 1, specificity ranged from 0.33 to 1, positive predictive values (PPV) ranged from 0 to 0.73, negative predictive values (NPV) ranged from 0.68 to 0.93. Cohen's kappa varied between 0 and 0.65 The poorest agreement was for the thermistor method, and the best agreement was obtained when a combination of thoraco-abdominal movements and nasal respiratory-airflow pressure was employed (sensitivity = 0.86, specificity = 0.83, PPV = 0.71, NPV = 0.92, Cohen's kappa = 0.65). We conclude that none of the indirect methods investigated, individually or in combination, proved adequate for identification of voluntary hypopneas in awake individuals.

Arousals and nocturnal respiration in symptomatic snorers and nonsnorers.

The purpose of the present investigation was to examine the relationship among upper airway resistance, snoring, and arousals, all measured simultaneously, in nonapneic snorers complaining of excessive daytime sleepiness (EDS). To accomplish this task, we selected a group of nine nonapneic snorers who presented because of snoring, EDS, tiredness, or fatigue. Ten healthy, alert, nonapneic, nonsnoring subjects recruited from among the hospital personnel acted as a comparison group. All subjects had nocturnal polysomnography, which included measurements of snoring, nasal and pharyngeal airway pressure, esophageal pressure, and total respiratory flow. Each polysomnogram was analyzed to identify all arousals and all respiratory events, i.e. apneas, hypopneas, and periods of increased upper airway resistance. Each arousal was examined to determine whether it was associated with a respiratory event, and each respiratory event was examined to determine whether it was associated with an arousal. The results were compared between snorers and nonsnorers. There was no significant difference between the two groups in the total sleep time (182+/-61 minutes in controls vs. 188+/-50 minutes in patients) or the total number of arousals per hour of sleep (24+/-12 in controls vs. 28+/-10 in snorers). However, the distribution of arousals, i.e. electroencephalogram (EEG) vs. respiratory, was different in snorers and nonsnorers. In snorers 55% of arousals were respiratory, whereas in nonsnorers only 17% of arousals were associated with respiratory events. Not unexpectedly, the snorers had significantly more respiratory events during the night (512) than controls (112). However, the relative proportion of these events that was accompanied by arousals was similar in both groups. We conclude that the difference in daytime function between symptomatic snorers and asymptomatic nonsnorers is unlikely to be due strictly to the number of arousals during the night; however, it is possible that respiratory and EEG arousals have different impacts on daytime performance, which may explain the difference in daytime function between our two groups.

Comparing perceptions and measurements of snoring.

The difficulty in measuring and quantifying snoring using objective criteria is that snoring is first and foremost of a subjective perception by a listener. To test the subjective perception of snoring and to compare it with objective measurements, we studied 25 patients referred to our laboratory because of snoring. All had full nocturnal polysomnography including measurements of snoring. Snoring sounds were recorded on paper and simultaneously stored on audiotape. The technologist scoring the polysomnogram counted the number of snores during a 20-minute segment. Two other technologists, unaware of the objective snoring count, listened to the audiotape and also counted the number of events that they perceived as snores. In 11 of 25 patients there was good agreement (within 25%) between the two listeners and the objective snore count. In another 7 of 25 patients there was good agreement between the listeners, but the objective snore count differed > 25%. In the last group of seven of 25 patients the difference in subjective snore counts perceived by both listeners was > 25%. The agreement between both listeners in judging snoring severity was moderate (weighted Cohen's kappa (w) = 0.49). We conclude that perception of snoring is highly subjective. We speculate that investigations studying consequences and treatment of snoring must employ either more sophisticated properly validated methods to measure snoring or alternatively resort to measurements of the underlying physiological abnormalities responsible for snoring, such as elevations in upper airway resistance.