Neck Grasp Predicts Obstructive Sleep Apnea in Type 2 Diabetes Mellitus.

AIMS: Obstructive sleep apnea (OSA) is a common disorder with high morbidity, mortality, and an increasing prevalence in the general population. It has an even higher prevalence among individuals with type 2 diabetes mellitus (DM). The snoring, tiredness, observed apnea, high blood pressure, body-mass-index, age, neck circumference and male gender (STOP-BANG) questionnaire and Berlin Questionnaire can be cumbersome in clinical practice and require subjective data on sleepiness. We proposed prospectively studying a primary care population with type 2 DM comparing neck grasp, neck circumference, and common screening questionnaires to identify OSA. METHODS: Persons with a diagnosis of type 2 DM were recruited from a primary care clinic. Participants were screened using Easy Sleep Apnea Predictor (ESAP), STOP-Bang questionnaire, and Berlin questionnaire. A positive ESAP was defined as a 1cm gap when a patient encircled their hands around the neck. All subjects underwent in-laboratory PSG testing. RESULTS: Forty-three participants were enrolled and the prevalence of OSA was 90.7% (AHI ≥ 5). The median BMI was 38.0. The prevalence of mild OSA by PSG (AHI 5-14) was 27.9%, moderate OSA (AHI 15-29) was 25.6%, and severe OSA (AHI >30) was 37.2%. For mild OSA both ESAP and neck circumference showed 100% specificity. CONCLUSIONS: This study reinforces the need for screening diabetic persons for obstructive sleep apnea. ESAP and neck circumference are useful for identifying persons with type 2 DM who are at risk for OSA. Together these findings could improve recognition of OSA in persons at risk for cardiovascular disease. Trial Registration of "Neck grasp as a predictor of Sleep Apnea," https://clinicaltrials.gov/ct2/show/NCT02474823, Clinical Trials.gov Identifier, is NCT02474823.

Severe hypercapnia after low-flow oxygen therapy in patients with neuromuscular disease and diaphragmatic dysfunction.

OBJECTIVE: To increase the general awareness of the possible exacerbation of hypercapnia by the administration of low-flow oxygen in patients with neuromuscular disorders. DESIGN: We retrospectively reviewed the medical records of 118 consecutive adult patients with a diagnosis of neuromuscular disease who underwent phrenic nerve conduction studies during a 5-year period, and we analyzed pulmonary function data for 8 patients who underwent arterial blood gas studies before and after the administration of low-flow oxygen. MATERIAL AND METHODS: In the eight patients with neuromuscular disease and diaphragmatic dysfunction (three with polymyositis, three with amyotrophic lateral sclerosis or nonspecific motor neuron disease, and one each with inflammatory motor neuropathy and chronic poliomyelitis), we analyzed the response of the arterial carbon dioxide tension (PaCO2) after low-flow supplemental oxygen therapy (0.5 to 2 L/min). Linear analysis was used to attempt to find correlations between respiratory variables and the PaCO2 response after oxygen therapy. RESULTS: For the overall study group, the mean PaCO2 increased 28.2 +/- 23.3 torr after low-flow oxygen treatment; in five patients, it increased by 27 torr or more. Four patients who were subsequently treated with nocturnal assisted ventilation were able to use supplemental oxygen during the day with less severe hypercapnia. Statistical analysis failed to reveal specific correlations between increased PaCO2 values after oxygen therapy and any respiratory variables. CONCLUSION: In patients with neuromuscular disease and diaphragmatic dysfunction, even low-flow supplemental oxygen should be administered with caution, and assisted ventilation should be strongly considered as an initial intervention.

The effects of transcutaneous electrical stimulation during wakefulness and sleep in patients with obstructive sleep apnea.

Upper airway (UA) collapse in obstructive sleep apnea (OSA) is considered in part to result from the decrease in UA dilator muscle tone that occurs during sleep. We hypothesized that augmentation of UA muscle function by transcutaneous electrical stimulation (TES) might function to enlarge UA size during wakefulness and/or prevent UA collapse during sleep in patients with OSA. Eight male patients with OSA were studied both awake and asleep, with TES administered to the submental region in two patients and to both the submental and subhyoid regions in six patients. Fast-CT scans obtained at FRC and end-inspiration (VTei) demonstrated increased UA size with tidal breathing, p less than or equal to 0.05. The active generation of -10 cm H2O pressure at FRC substantially decreased UA size, p less than or equal to 0.001. However, no changes in UA size were detected at either FRC or VTei with TES applied at 50 and 100% of the maximal tolerated intensity. The collapsibility of the UA in response to the generation of -10 cm H2O pressure was also unchanged by TES. In contrast to the lack of effect of TES on UA size, voluntary protrusion of the tongue increased cross-sectional area (CSA) of the orohypopharyngeal (OHP) segment of the UA, p less than 0.05, and to a lesser extent the CSA of the distal velopharyngeal segment, p = 0.06. When applied during sleep, TES failed to prevent or improve either sleep-disordered breathing or sleep architecture.(ABSTRACT TRUNCATED AT 250 WORDS)

Syphilis: a disease to exclude in diagnosing sarcoidosis.

A 37-year-old man was referred to our institution for assessment of possible sarcoidosis with involvement of the central nervous system. Before referral, he experienced a systemic illness that persisted for several months, during which time ocular and pulmonary noncaseating granulomas were identified. Sarcoidosis with involvement of the central nervous system was tentatively diagnosed. Because of several inconsistencies in the preliminary diagnosis of sarcoidosis, further assessment was pursued, and syphilis was diagnosed. Herein we emphasize the useful clinical features for distinguishing syphilis from sarcoidosis and review the clinical manifestations of pulmonary syphilis.

Effect of variation in infusion time and macrophage blockade on organ uptake of amphotericin B-deoxycholate.

Amphotericin B is administered as a colloidal suspension due to its insolubility in water. Macrophages, particularly those in the liver, have been implicated as the predominant cell type responsible for the uptake of colloidal amphotericin B. We examined the effect of infusion time and macrophage function to confirm the role of the macrophage in the uptake of amphotericin B. Prolonged infusion time (24 h compared to 6 h) resulted in significantly less hepatic and splenic accumulation of amphotericin B. Blockade of macrophage function with methylpalmitate also resulted in significantly decreased hepatic and splenic uptake of amphotericin B. Uptake of amphotericin B by lung macrophages was not significantly affected by methylpalmitate. The area under the serum concentration versus time curve was significantly higher in the group that received methylpalmitate compared to either the 6 or 24 h amphotericin B infusion groups. These results suggest that fixed macrophages play an important part in the pharmacokinetics of amphotericin B, and that increasing drug solubility may alter the pharmacokinetics of amphotericin B.

Solubility and stability of amphotericin B in human serum.

The solubility and stability of amphotericin B in human serum in vitro was assessed using a sensitive high performance liquid chromatographic technique. The solubility of amphotericin B at concentrations ranging from 0.5 micrograms/ml to 10 micrograms/ml in human serum at pH 7.4, at 37 degrees C, and in 5% CO2 (simulated in vivo conditions) showed no significant difference compared with the solubility at 23 degrees C in room air after a 1 h incubation period. Dissolution of the colloidal suspension at a concentration of 2 micrograms/ml reached 81% in 3 min with a small increase in solubility by 60 min. Amphotericin B was very stable (less than 5% loss) in human serum at -20 degrees C for up to 14 days with only a 10% loss of drug at 6 months. In dimethylsulfoxide, however, losses at 6 months were greater than 60%. We conclude that amphotericin B solubilizes, but not completely, from a colloidal form in human serum under simulated in vivo conditions at 37 degrees C and at 23 degrees C in room air over 1 hour. Additionally, amphotericin B is stable in frozen serum for 6 months.

Protective actions of a new thromboxane synthetase inhibitor in arachidonate induced sudden death.

A new thromboxane synthetase inhibitor, OKY-046, at doses of 0.5 and 1.0 mg/kg prevented mortality induced by sodium arachidonate in 100% of the rabbits studied. Sodium arachidonate at a dose of 1.25 mg/kg uniformly decreased mean arterial blood pressure to values approximately 0 mm Hg, stopped respiration and produced sudden death within 3-5 minutes in all rabbits studied. OKY-046 prevented all these sequelae of the sodium arachidonate. Untreated rabbits challenged with sodium arachidonate develop large increases in circulating thromboxane B2 (TxB2) and 6-keto PGF1 alpha of about 12- to 18-fold. In contrast, OKY-046 prevented the increase in TxB2 concentrations and the pulmonary thrombosis, but did not block the rise in 6-keto PGF1 alpha following arachidonate injection. These results suggest that the protective mechanism of OKY-046 in arachidonate induced sudden death is via selective inhibition of thromboxane synthesis.