Incidental anaesthesia during pregnancy

html xmlns=”http://www.w3.org/1999/xhtml” xmlns:mml=”http://www.w3.org/1998/Math/MathML” xmlns:epub=”http://www.idpf.org/2007/ops”>


Chapter 8 Incidental anaesthesia during pregnancy


Desiree M. A. Choi and Kim G. Soulsby



Introduction


Parturients may require anaesthesia during their pregnancy in order to facilitate obstetric or non-obstetric surgical procedures. Common obstetric procedures required in pregnancy include cervical cerclage, ovarian cyst interventions and fetal surgery. The incidence of incidental or non-obstetric anaesthesia in pregnancy has been reported as ranging from 1:50–150 pregnancies, with appendectomy, cholecystectomy and pelvic laparoscopy being the most commonly encountered procedures.


Incidental anaesthesia must minimize the risk of interrupting the pregnancy and affecting fetal development. Alterations in maternal physiology accentuate anaesthetic risks and the approach to anaesthesia must be modified accordingly.



Fetal considerations


Anaesthesia may impact on the fetus in two ways: it may interrupt the pregnancy, resulting in either pregnancy loss or premature delivery, or it may impact on fetal development, either by teratogenic pharmacological effects or because of derangements in the physiological milieu.


The effects of a teratogenic insult depend on the gestation of the fetus at the time of exposure. Teratogens cause an ‘all or nothing’ effect in the early pluripotential developmental phase, such that the embryo will either die or be unaffected and develop normally. However, days 31 to 71 of human gestation correspond to the organogenesis phase, where exposure to teratogens may impair the structural development of organ systems. First trimester anaesthesia has been linked with increased neonatal central nervous system and eye malformation, particularly hydrocephalus and cataracts. In the phase following organogenesis, teratogen exposure is more likely to affect the fetal central nervous system, which undergoes development and maturation throughout pregnancy. These effects are likely to result in functional behavioural effects rather than structural malformations.



Drug teratogenicity



Organogenesis phase


There is theoretical reason to suspect that drugs used in anaesthesia may be teratogenic: the cellular mechanisms for differentiation and organogenesis include mechanisms known to be targeted by drugs used in anaesthesia. Neurotransmitter and receptor mechanisms, as well as signalling and second messenger systems are all known to be affected by drugs used in anaesthesia. This theoretical risk of teratogenicity has been difficult to quantify in a practical clinical context, because of difficulties extrapolating animal research data to human development (teratogenicity is species specific) and the obvious ethical and logistical problems of research on human fetal exposure to teratogens.



Later pregnancy


Drugs used in later pregnancy may have direct effects other than structural organogenesis impairment.


Benzodiazepines in late pregnancy may result in fetal benzodiazepine dependence and withdrawal (although unlikely in the short-term context of a single anaesthetic). Used peripartum, they are associated with fetal hypotonia, respiratory depression and hypothermia, and are probably best avoided in a viable gestation pregnancy.


Opioids have similar potential for fetal dependence and withdrawal, but again this is unlikely to result from short-term anaesthetic use. Peripartum opioid use results in reversible respiratory depression.


Non-steroidal anti-inflammatory drugs in the third trimester have been linked to premature closure of the ductus arteriosus, tricuspid incompetence and pulmonary hypertension. They have been associated with a range of fetal and neonatal effects consistent with their side-effect profile (including platelet dysfunction and intracranial haemorrhage, renal impairment and gastrointestinal bleeding), and their use should be avoided after 32 weeks’ gestation.


Neuromuscular blocking agents are polar molecules that do not readily cross the maternal–placental barrier and are safe to use in late pregnancy.


The antiemetic prochlorperazine has been associated with neonatal jaundice and extrapyramidal side effects when used in high dose late in pregnancy.



Fetal effects of deranged maternal physiology



Organogenesis phase


There is some evidence that chronic hypercarbia and hyperthermia may be teratogenic, but it seems unlikely that anaesthesia would result in such exposure.



Later pregnancy


Derangements in maternal physiology that are precipitated or exacerbated by anaesthesia are likely to impact on the fetus by their effects on uteroplacental perfusion and oxygen delivery. Regardless of the cause of reduced uteroplacental perfusion, the fetal effects are similar: acidosis and fetal hypoxaemia will result. The insult may result in fetal injury, ranging from transient mild acidosis or hypoxaemia to brain injury, and ultimately to fetal death if the injury is unrecognized or untreated.



Uteroplacental blood flow


Reduced uteroplacental blood flow results most commonly from aortocaval compression, and is preventable with careful positioning during anaesthesia. Unrecognized and untreated reduction in circulating volume (whether absolute, as in haemorrhage, or relative as in sepsis) will reduce placental perfusion, and may do so without overt maternal hypotension because of the additional mobilized cardiac reserve in pregnancy.



Oxygen homeostasis


Fetal compensation to moderate, transient maternal hypoxaemia occurs by increased oxygen extraction, and may be well tolerated by the healthy fetus. This compensation is facilitated by fetal haemoglobin HbF, which has a high affinity for oxygen and which avidly binds maternal oxygen. However, an acidotic fetus will demonstrate a rightward shift in the oxygen dissociation curve, with reduced affinity for maternal oxygen. An acidotic fetus does not tolerate maternal hypoxia well.


In severe maternal hypoxia the maternal compensatory response is to divert flow to vital maternal organs, and away from the placenta. Uterine vasoconstriction results, reducing oxygen delivery to the fetus.



Carbon dioxide homeostasis


Carbon dioxide and its effects on acid–base balance may affect the fetus directly, by diffusing into the fetal circulation, and indirectly by the affecting uterine blood flow. Maternal hypercarbia results directly in fetal hypercarbia and respiratory acidosis. This results in a rightward shift in the fetal oxygen dissociation curve, with a consequent reduction in fetal oxygen extraction, leaving the fetus vulnerable to the effects of co-existent hypoxia. Fetal hypercarbia and acidosis also impair fetal myocardial contractility.


Maternal hypercarbia results in uterine vasodilation and increased uteroplacental flow, although severe hypercarbia may reduce uteroplacental flow by causing vasoconstriction. Maternal hypocarbia is poorly tolerated by the fetus, because hypocarbia and alkalaemia result in uterine vasoconstriction, reducing uteroplacental blood flow.



Miscarriage and premature delivery


The evidence for an increased risk of miscarriage following anaesthesia and surgery in pregnancy comes mainly from large retrospective studies of pregnancy outcomes following incidental surgery and anaesthesia. Further evidence is extrapolated from epidemiological studies linking occupational exposure to nitrous oxide and volatile anaesthetic agents with increased miscarriage rates.


Brodsky et al. showed an increase in the spontaneous abortion rate from the baseline of 5.1% to 8% in the first trimester pregnancies following anaesthesia and surgery. This seemed to be unrelated to the site of surgery, and abdominal and pelvic surgery was not more likely than remote surgery to induce miscarriage.


The increase in spontaneous abortion in the second trimester from 1.4% baseline to 5.9% was shown in pregnancies exposed to incidental surgery and anaesthesia, again irrespective of the anatomical site of surgery.


Once a pregnancy is of viable gestation, incidental surgery and anaesthesia may increase the risk of premature labour and delivery. This appears to be higher for gynaecological and abdominal surgery, which involves manipulation of the uterus. A systematic review found the rate of premature delivery following non-obstetric surgery to be 3.5%, with appendectomy carrying the highest risk of premature delivery. The trend towards the use of laparoscopic techniques in parturients has raised concerns regarding the risk of direct injury from laparoscopic instruments, and from indirect effects of hypercarbia and pneumoperitoneum. However, a number of subsequent studies have suggested that laparoscopy is not associated with increased risk of pregnancy loss or poor fetal outcome.

Only gold members can continue reading. Log In or Register to continue

Jan 28, 2017 | Posted by in ANESTHESIA | Comments Off on Incidental anaesthesia during pregnancy
Premium Wordpress Themes by UFO Themes