Contraceptive Options Following Gestational Diabetes: Current Perspectives.

Gestational diabetes mellitus (GDM) complicates approximately 7% of pregnancies in the United States. Along with risk factors related to pregnancy, women with a history of GDM also have an increased risk of developing type 2 diabetes mellitus later in life. These women require special consideration when discussing contraception and other reproductive health issues. GDM carries a category 1 rating in the US Medical Eligibility Criteria for all contraceptive methods, which supports safety of the various methods but does not account for effectiveness. Contraceptive options differ in composition and mechanisms of action, and concerns have been raised about possible effects of contraception on metabolism. Clinical evidence is limited to suggest that hormonal contraception has significantly adverse effects on body weight, lipid, or glucose metabolism. In addition, the majority of evidence does not suggest a relationship between development of type 2 diabetes mellitus and use of hormonal contraception. Data are limited, so it is challenging to make a broad, general recommendation regarding contraception for women with a history of GDM. A woman's history of GDM should be considered during contraceptive counseling. Discussion should focus on potential medical comorbidities and the implications of GDM on future health, with special consideration of issues including bone health, obesity, cardiovascular disease, and thrombosis risk. Providers must emphasize the importance of reliable, highly effective contraception for women with GDM, to optimize the timing of future pregnancies. This approach to comprehensive counseling will guide optimal decision-making on contraceptive use, lifestyle changes, and planning of subsequent pregnancies.

State-specific effects of sevoflurane anesthesia on sleep homeostasis: selective recovery of slow wave but not rapid eye movement sleep.

BACKGROUND: Prolonged propofol administration does not result in signs of sleep deprivation, and propofol anesthesia appears to satisfy the homeostatic need for both rapid eye movement (REM) and non-REM (NREM) sleep. In the current study, the effects of sevoflurane on recovery from total sleep deprivation were investigated. METHODS: Ten male rats were instrumented for electrophysiologic recordings under three conditions: (1) 36-h ad libitum sleep; (2) 12-h sleep deprivation followed by 24-h ad libitum sleep; and (3) 12-h sleep deprivation, followed by 6-h sevoflurane exposure, followed by 18-h ad libitum sleep. The percentage of waking, NREM sleep, and REM sleep, as well as NREM sleep δ power, were calculated and compared for all three conditions. RESULTS: Total sleep deprivation resulted in significantly increased NREM and REM sleep for 12-h postdeprivation. Sevoflurane exposure after deprivation eliminated the homeostatic increase in NREM sleep and produced a significant decrease in the NREM sleep δ power during the postanesthetic period, indicating a complete recovery from the effects of deprivation. However, sevoflurane did not affect the time course of REM sleep recovery, which required 12 h after deprivation and anesthetic exposure. CONCLUSION: Unlike propofol, sevoflurane anesthesia has differential effects on NREM and REM sleep homeostasis. These data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.

Isoflurane anesthesia does not satisfy the homeostatic need for rapid eye movement sleep.

BACKGROUND: Sleep and general anesthesia are distinct states of consciousness that share many traits. Prior studies suggest that propofol anesthesia facilitates recovery from rapid eye movement (REM) and non-REM (NREM) sleep deprivation, but the effects of inhaled anesthetics have not yet been studied. We tested the hypothesis that isoflurane anesthesia would also facilitate recovery from REM sleep deprivation. METHODS: Six rats were implanted with superficial cortical, deep hippocampal, and nuchal muscle electrodes. Animals were deprived of REM sleep for 24 hours and then (1) allowed to sleep ad libitum for 8 hours or (2) were immediately anesthetized with isoflurane for a 4-hour period followed by ad libitum sleep for 4 hours. The percentage of REM and NREM sleep after the protocols was compared with similar conditions without sleep deprivation. Hippocampal activity during isoflurane anesthesia was also compared with activity during REM sleep and active waking. RESULTS: Recovery after deprivation was associated with a 5.7-fold increase (P = 0.0005) in REM sleep in the first 2 hours and a 2.6-fold increase (P = 0.004) in the following 2 hours. Animals that underwent isoflurane anesthesia after deprivation demonstrated a 3.6-fold increase (P = 0.001) in REM sleep in the first 2 hours of recovery and a 2.2-fold increase (P = 0.003) in the second 2 hours. There were no significant differences in REM sleep rebound between the first 4 hours after deprivation and the first 4 hours after both deprivation and isoflurane anesthesia. Hippocampal activity during isoflurane anesthesia was not affected by REM sleep deprivation, and the probability distribution of events during anesthesia was more similar to that of waking than to REM sleep. CONCLUSION: Unlike propofol, isoflurane does not satisfy the homeostatic need for REM sleep. Furthermore, the regulation and organization of hippocampal events during anesthesia are unlike sleep. We conclude that different anesthetics have distinct interfaces with sleep.