This was a prospective observational study to identify the incidence and possible risk factors for maternal desaturation following neuraxial blockade for elective caesarean section (CS). Patients with body mass index (BMI) ≥ 30 kg/m2 at the first antenatal consultation were identified and classified into the obese group. Neuraxial blockade in the form of subarachnoid block (SAB) or combined spinal-epidural (CSE) was performed. Mean arterial pressure (MAP) and oxygen saturation (SpO2) were recorded at baseline and at 5-minute intervals following neuraxial blockade. Desaturation, defined as SpO2 < 94% for more than 30 seconds without artifacts, was managed with oxygen therapy and other appropriate measures. Newborn Apgar score and umbilical cord blood gases were analysed. Among a total of 254 recruited patients, 69 (27.2%) were obese and were associated with significantly higher age, parity, previous CS and pre-existing diabetes mellitus. The incidence of oxygen desaturation was 1.2%, involving three patients in the non obese group. These desaturation episodes were short-lived and associated with intraoperative hypotension. Six patients, two of whom in the obese group, received rescue oxygen therapy following intraoperative events such as deteriorating SpO2 or hypotension. The mean MAP was significantly lower at baseline and at 5 minutes post neuraxial blockade in the non obese group, which could account for the occurrence of desaturation in this group only. There were no significant inter-group differences in terms of neonatal outcome, umbilical cord blood gases and changes in mean SpO2 post neuraxial blockade. In conclusion, the current practice of not routinely giving supplementary oxygen to patient during elective CS at our institution is deemed to be safe, provided continuous SpO2 monitoring is available throughout the surgery. Further randomised clinical trials are indicated to investigate the impact of maternal obesity and of labouring patients presenting for urgent or emergency CS on intraoperative oxygen desaturation.
Although leptin has been shown to increase blood pressure (BP), it is however unclear if this increase can be prevented by exercise. This study therefore investigated the effect of leptin treatment with concurrent exercise on blood pressure (BP), sodium output, and endothelin-1 (ET-1) levels in normotensive rats. Male Sprague-Dawley rats weighing 250-270 g were divided into four groups consisting of a control group (n = 6), leptin-treated (n = 8), non-leptin-treated exercise group (n = 8), and a leptin-treated exercise group (n = 8). Leptin was given subcutaneously daily for 14 days (60 μg/kg/day). Animals were exercised on a treadmill for 30 min at a speed of 0.5 m/s and at 5° incline four times per week. Measurement of systolic blood pressure (SBP) and collection of urine samples for estimation of sodium and creatinine was done once a week. Serum samples were collected at the end of the experiment for determination of sodium, creatinine and ET-1. At day 14, mean SBP and serum ET-1 level in the leptin-treated group was significantly higher than that in the control group whereas mean SBP and serum ET-1 level was significantly lower in the leptin-treated exercise group than those in leptin-treated and control groups. Creatinine clearance, urinary sodium excretion, and urine output were not different between the four groups. Regular treadmill exercise prevents leptin-induced increases in SBP in rats, which might in part result from increased urinary sodium excretion and preventing the leptin-induced increases in serum ET-1 concentration.