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Tags: Obstetrics, Neuraxial block

Epidural hyperthermia

Epidural hyperthermia, also known as epidural-related fever, refers to the situation in which a parturient who has an epidural for labour analgesia develops an increased body temperature

It was first reported in 1989 when vaginal temperature was compared between parturients who received either pethidine or epidural analgesia: the temperature did not change in those who received pethidine but increased at 0.15°C h−1 in those who received epidural analgesia

Intrapartum hyperthermia is the umbrella term for any increased maternal temperature during labour.

During an uncomplicated labour, maternal metabolic rate increases by 25%, but this does not result in a significant change in body temperature.

Consequently, a commonly used definition of intrapartum hyperthermia is: ‘a core temperature during labour of ≥38°C on one occasion or ≥37.5°C on two consecutive occasions two hours apart’.

Epidural hyperthermia and intrapartum infection are the two major aetiologies

incidence of intrapartum hyperthermia is 20% in parturients with epidural analgesia and 5% in those without

In parturients with epidural analgesia intrapartum, hyperthermia may be secondary to infection or a direct result of the epidural itself
Epidural analgesia does not increase the risk of intrapartum infection

Tachypnoea, tachycardia, and leukocytosis may all occur in the absence of intrapartum infection, and as a result intrapartum hyperthermia alone is considered sufficient evidence to initiate maternal sepsis evaluation and antibiotic administration

currently it is not possible to differentiate cases of epidural hyperthermia that are caused by intrapartum infection from cases that are a consequence of the epidural itself

Consequences

preliminary evidence points to a link with an increased risk of neonatal brain injury

Evaluation and investigation for sepsis, and antibiotic treatment are both established consequences
It is also associated with an increased risk of both Caesarean and instrumental delivery, although these correlations may be coincidental

Epidural hyperthermia is associated with a two-fold increase in the risk of Caesarean delivery and instrumental vaginal delivery.

However, it is not clear if this association signifies a causal link or is a coincidence

Epidural hyperthermia increases the risk of labour arrest, rather than the risk of maternal or fetal distress, and so it is unlikely that the increased incidence of operative delivery is attributable to clinical concerns for intrapartum infection

Chorioamnionitis impairs myometrial contractility and thus increases the risk of labour arrest and operative delivery. It is possible that epidural hyperthermia has a similar effect on myometrial contractility, but this explanation is untested

Epidural hyperthermia is a time-dependent condition; that is maternal temperature increases at a constant rate after epidural insertion

Mechanisms

The mechanism underlying epidural hyperthermia is uncertain.

A number of mechanisms have been hypothesised, including

two leading theories have emerged: sympathetic blockade and immunomodulation

Symapthetic blockade hypothesis

The sympathetic blockade hypothesis is that epidural analgesia ==limits cutaneous heat loss ==via blockade of active cutaneous vasodilation and sweating

Heat loss is regulated by two pathways of the sympathetic nervous system:

effect of neuraxial blockade on body temperature is dependent upon body temperature before block placement

Before elective Caesarean delivery or non-obstetric surgery, patients are in a thermoneutral state and so neuraxial blockade blocks active vasoconstriction resulting in increased heat loss and a reduction in body temperature

neural blockade during established hyperthermia blocks active vasodilation and sweating resulting in decreased heat loss.
Labour is a heat stress, and so it is plausible that the sympathetic blockade associated with intrapartum epidural analgesia would limit heat loss

Immunomodulation hypothesis

The immunomodulation hypothesis is that epidural administration of local anaesthetic during labour provokes a sterile febrile response

epidural hyperthermia occurs in conjunction with a proinflammatory state, but it is unclear if this proinflammatory state is induced by epidural analgesia or if it is a confounder

In parturients without epidural analgesia, activation of the pyrogenic pathway via activated caspase-1 (casp1), interleukin-1β (IL-1β), and interlukin-6 (IL-6) is attenuated by the parallel release of the antipyrogenic cytokine interleukin-1 receptor antagonist (IL1-ra).
In parturients receiving epidural analgesia, inhibition of caspase-1 activity reduces the release of IL1-ra


References

Hyperthermia after epidural analgesia in obstetrics - BJA Education
Hyperthermia After Epidural Analgesia in Obstetrics - BJA Ed