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Body temperature, heat balance and skin blood flow before and after epidural extension for emergency caesarean section: an investigation of the mechanism underlying epidural hyperthermia

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Body temperature, heat balance and skin blood flow before and after epidural extension for emergency caesarean section. An investigation of the mechanism underlying epidural hyperthermia.

•Epidural analgesia for labour is frequently (up to 46%) complicated by hyperthermia (core temperature > 38°C)1.
•Epidural hyperthermia is associated with adverse neonatal neurological outcome2.
•Labour is a heat stress (heat production is increased)1 and so a potential explanation is that epidural analgesia limits cutaneous heat loss via blockade of sympathetically mediated active cutaneous vasodilation3.
•Blockade of active vasodilation may be inferred if following epidural insertion either cutaneous heat loss4 or skin blood flow2 decrease.
•It is difficult to test this hypothesis directly as the pain of labour impedes data collection before epidural insertion.
•A solution is to test the hypothesis during epidural extension for emergency caesarean section where labour is on-going and data can be collected before and after an increment in the distribution of neural blockade.
 
Aim: to investigate the mechanism underlying epidural hyperthermia by examining the change in cutaneous vascular tone associated with epidural extension for emergency caesarean section.
Hypothesis: epidural extension blocks active vasodilation (cutaneous heat loss and skin blood flow decrease) and as a result heat production exceeds heat loss and mean body temperature rises.
•20 patients (age 33 (5) years, BMI 26 (23 – 29) kg.m-2) in established labour received standardised epidural extension for emergency caesarean section with lignocaine-bicarbonate-adrenaline solution.
•The following were recorded for five minutes before epidural extension and continuously thereafter until the end of the caesarean section:
–Core temperature (thermocouple): aural canal.
–Skin temperature (thermocouples): area weighted mean of head, chest, forearm, finger, thigh, calf and toe.
–Cutaneous heat loss (heat flux sensors): area weighted mean of head, chest, forearm, thigh and calf.
–Skin blood flow (laser doppler flowmetry): arm and thigh.
•Mean body temperature and heat production were calculated.
•Data are mean (SD) and median (IQR) as appropriate. Temperatures at three time points (T -block: when sensory blockade was adequate for surgery; TOB: time of birth; End: end of surgery) and the average values of heat production, heat loss and skin blood flow over 2 intervals (T-block – TOB and TOB – End) were compared to their values before epidural extension (Before) with RM ANOVA (Holm-Sidak post hoc analysis).
•This study is the first time that temperature, heat balance and skin blood flow have been recorded during emergency caesarean section.
•Epidural extension limited cutaneous heat loss and as a result until delivery mean body temperature increased at 0.5°C.h-1.
•The most likely explanation for the cutaneous heat loss limitation is blockade of active vasodilation4. The lack of change in skin blood flow does not refute this explanation. During heat stress skin blood flow is subject to competing cholinergic and noradrenergic reflexes and so the effect of sympatholysis is unpredictable3.
•It is possible that epidural analgesia for labour blocks active cutaneous vasodilation over a smaller proportion of the body surface. Consequently, epidural hyperthermia may be a result of sympathetic blockade.
•Following delivery heat production decreased and so mean body temperature fell. This reduction in heat production is likely due to the separation of the feto-placental unit and the cessation of uterine contractions.
•Patients were hyperthermic throughout and so the routine use of active warming during emergency caesarean section should be reviewed.
•Future work should directly test cutaneous sympathetic nerve activity in healthy heat stressed populations.
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