202406151741

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Tags: Paed, Obstetrics

Foetal anaesthesia

4 categories

Conduct of anaesthesia

Aim

From gestational age 15-18wks

The inspired oxygen concentration should not surpass 35%, as higher values might elevate the presence of free oxygen radicals and the target maternal paCO2 should be maintained around 30 mmHg, a level considered as physiologic in pregnant women.

human uterus lacks autoregulation

To prevent uterine (and placental) hypoperfusion, it is advised to maintain maternal blood pressure at physiological levels (around 70–90% of baseline, or a mean arterial pressure >65 mmHg). This can be achieved by administering vaso-active drugs like phenylephrine or noradrenaline (ephedrine is used in cases of maternal bradycardia), providing intravenous fluids, avoiding excessively deep levels of general anaesthesia, and positioning the patient avoiding caval compression (preferably in left lateral tilt position of ≥30°) from 10 to 18 weeks of gestation

there is a notable decrease of 30–40% in the minimum alveolar concentration (MAC) of volatile anaesthetic agents from around 8 weeks [23]. Nevertheless, instances of awareness are more prevalent in the pregnant population (1 in 670 during general anaesthesia for caesarean section) compared to the general population (1 in 19,600)

While neostigmine has been used for many years, it can lead to foetal bradycardia, necessitating the co-administration of atropine

glycopyrrolate, unlike neostigmine, does not cross the placenta and therefore cannot prevent foetal bradycardia

Pain → ↓uterine blood flow → premature contraction
∴ post-op analgesia important

VTE risks

Sustaining an adequate intrauterine volume by continuously replenishing lost amniotic fluid is also imperative during the perioperative period to avert severe uterine contractions

In the 1980s, the medical consensus leaned towards the belief that foetuses and even newborns lacked the capacity to experience pain due to the underdeveloped cerebral cortex

In the 1990s, it was noted that nociceptive stimuli in the foetus triggered the hypothalamo-pituitary-adrenal axis and the sympathetic nervous system [60,68,69]. However, using this stress response as a sole indicator for foetal pain had limitations: it did not involve the cortex, and responses like exercise, hypoxia, or haemorrhage could elicit similar reactions

Later it was suggested that foetal pain perception required the transmission of pain stimuli from peripheral nociceptors to the somatosensory cortex [70,71]. This pathway, functional only from 24 weeks of gestation, implied that pain perception might only begin at this stage

Responses before 24 weeks were viewed as reflexes rather than indicative of pain perception

the latest evidence suggests that thalamic connections to the subplate, forming as early as 12 weeks of gestation, might be functionally equivalent to thalamocortical connections [68,70,71]. The subplate, a transient layer in the developing cerebral cortex, acts as an active precursor to the cortex [68,70]. Consequently, the emerging view is that foetal pain perception might occur as early as 12 weeks of gestation

While volatile anaesthetics and propofol, critical components of foetal anaesthesia, cross the placenta, their foetal concentrations, even after prolonged administration, reach only around 70% and 50% of maternal concentrations, respectively [70,72]. This level may not suffice for foetal surgery

Procedures painful to foetus or need foetal immobilisation:

Procedures NOT painful to foetus:

route of foetal drug admin

Intravascular administration offers a rapid onset of action and can be achieved through the umbilical vein, large foetal veins, or intracardiacally, depending on the procedure [72]. However, this method presents potential disadvantages such as vessel thrombosis, vascular spasm, bleeding, and a possible compromise of the surgical view [72]. Accessing these routes can also be more challenging compared to other methods

neurodevelopment of foetus

The groundbreaking work by Ikonomidou et al., in 1999 demonstrated the widespread neuronal apoptosis in foetal and neonatal rats by blocking NMDA receptors using dizocilpine [73]. This study laid the foundation for the hypothesis that exposure to general anaesthesia during brain development might significantly impact neurodevelopmental outcomes

In response to this growing body of evidence, in 2016, the Food and Drug Administration (FDA) issued a warning emphasizing that repeated or prolonged exposure to general anaesthesia during the third trimester of pregnancy might have adverse effects on neurodevelopment

One notable limitation lies in the discrepancies between the duration, frequency, and doses of anaesthesia used in animal studies compared to typical clinical scenarios

Neurological impairments were observed with repeated exposures, doses surpassing one MAC (minimum alveolar concentration), or durations extending beyond 3 h. A single exposure at or below 1 MAC for up to 3 h did not yield significant impairments. It is crucial to contextualize the duration of exposure concerning the animal's pregnancy duration: for instance, exposure to 3 h of anaesthesia in rats, mice, non-human primates, sheep, rabbits, and guinea pigs would roughly equate to 37, 43, 5, 6, 27, and 12 h of anaesthesia in humans, respectively

Another limitation was the absence of surgical stimulation during most animal exposures to anaesthesia, which does not mirror clinical procedures where anaesthesia is often coupled with surgical interventions

the animal studies generally fell short in terms of monitoring and maintaining physiological stability, not reaching the clinical standards expected in human settings.

Clinical data on the effects of prenatal anaesthesia exposure and surgery are available only for maternal non-obstetric surgery (but not for foetal surgery)

References

Advances in Foetal Anaesthesia