202410240250
Status:
Tags: Obstetrics, Paed
Maternal-fetal intevention
3 main types:
- minimally invasive maternal–fetal interventions
- typically performed in early or midgestation
- open maternal–fetal surgery
- ex utero intrapartum treatment (EXIT) procedures
Pre-op
Pertinent information for the anesthesiologist includes gestational age, fetal cardiac function, estimated fetal weight for drug dosing, and placental location, which determines patient positioning and the need to exteriorize the uterus
Crisis plan
should also discuss the plan for the fetus in the event of an intraoperative maternal arrest and/or the need for fetal resuscitation. If the fetus is of a previable gestational age or the patient has elected not to resuscitate the fetus if born at the time of surgery, planning for emergent cesarean delivery is still needed, as it may be performed for maternal hemorrhage or cardiac arrest
Uterotonics should be readily available in the event of an unplanned cesarean delivery to prevent uterine atony
Fetal physiology
More than half of the fetal blood volume resides in the placenta and is approximately 110–160 mL/kg, from the start of the 2nd trimester to term
Fetal cardiac output is mainly a function of fetal heart rate (FHR). This is because the fetal myocardium is less compliant than adult myocardium and less responsive to fluctuations in preload
Right ventricular and left ventricular output are not equivalent in the fetus, so cardiac output is described in terms of the combined cardiac output (CCO) of both ventricles. A normal fetus has a CCO of 425–550 mL/kg/min
During surgical procedures resulting in significant fetal blood loss, the degree of hypovolemia and transfusion end point requires vigilant monitoring of both FHR and intraoperative fetal cardiac function using echocardiography
Fetal lungs are fluid filled, and the pulmonary epithelium secretes approximately 100 mL/kg/d of fluid that exits the fetal trachea to be either swallowed or introduced into the amniotic fluid
Although immature, the fetal liver synthesizes coagulation factors. These coagulation factors do not cross the placenta and are in lower concentration and less effective in forming clots compared to adults
Although fetal hepatic enzymes are less functional than in adults, most medications in the umbilical vein undergo a significant amount of fetal hepatic metabolism (first-pass metabolism) before circulating to the fetal brain or heart.
Fetal pharmacology
Molecules smaller than approximately 1000 Daltons are primarily exchanged between the maternal and fetal circulation by placental diffusion
The degree and rate of transfer are determined by
- transplacental concentration gradients,
- molecular weight,
- protein binding,
- ionization,
- lipid solubility
All drugs cross the placental barrier to some degree, but a few are significantly restricted. Examples of medications with severely limited maternal–fetal transfer include nondepolarizing neuromuscular blockers, succinylcholine, glycopyrrolate, unfractionated heparin, low-molecular-weight heparins, and insulin
Volatile anesthetics, opioids, benzodiazepines, and atropine readily cross the placenta.
Fetal analgesia
Direct fetal interventions, including the passage of a needle into the fetus, result in a hormonal stress response that is decreased with fetal opioid administration
Although pituitary–adrenal, sympathoadrenal, and nociceptive components of the stress response are present by 19 weeks’ gestation allowing a fetus to reflexively withdraw from a noxious stimulus without input from the cerebral cortex, thalamocortical connections to the somatosensory cortex allowing the perception of pain are not significantly developed until 24 to 30 weeks’ gestation
Because it remains uncertain exactly when a fetus has the capacity to feel pain, it is best to administer adequate fetal anesthesia in all invasive maternal–fetal procedures to inhibit the humoral stress response, decrease fetal movement, and blunt any perception of pain, as has been standard practice since the start of maternal–fetal surgery in the early 1980s
Opioid analgesics can reach the fetal circulation by maternal administration, direct fetal intramuscular administration, or intravenous umbilical cord administration
The umbilical cord and placenta have no known pain receptors, so procedures that only involve these tissues (eg, intrauterine transfusion or laser ablation for twin-to-twin transfusion syndrome) do not require fetal administration of analgesics. In these procedures, maternal opioid administration (eg, remifentanil) and subsequent placental transfer can assist with fetal immobility, but this is not always required
For open maternal–fetal procedures, the use of maternal general anesthesia allows the transfer of anesthetics from the mother to the fetus, but direct fetal administration of opioid is still required to blunt the fetal stress response to invasive procedures reliably
Maternal safety is paramount, and an assessment of fetal/neonatal risks and benefits of each maternal–fetal intervention must be weighed against potential maternal complications
Minimally invasive interventions
An anterior placenta might necessitate the lateral positioning of the patient for the procedure
Only minimal-to-moderate sedation should be used in either monitored anesthesia care or neuraxial anesthesia to preserve airway reflexes and maintain a level of consciousness so the patient can be directed to reposition herself or hold still during the procedure.
mild airway obstruction can occur if the mother becomes too sedated, and paradoxical motion of her chest and abdomen can create poor operative conditions.
Although preoperative tocolytics may be administered, profound intraoperative uterine relaxation is not necessary for minimally invasive procedures, and maternal administration of sedatives and analgesics only provides limited fetal analgesia via transplacental transfer
For more invasive maternal–fetal interventions, such as percutaneous balloon valvuloplasty or fetoscopic endoluminal tracheal occlusion, fetal analgesia is provided using an intramuscular or intraumbilical venous administration of a fetal mixture containing opioid and muscle relaxant, often accompanied with atropine to minimize the risk of fetal bradycardia.
In the past, intraoperative fluid administration was restricted secondary to concerns of maternal pulmonary edema from the absorption of irrigation fluids. However, judicious use and close accounting of intrauterine irrigation fluids have mitigated this issue, and routine maintenance fluids should be administered based on the patient’s volume status and the duration of surgery
Open fetal surgery
Crystalloid fluids are often used in restricted volumes (500–1000 ml), as mothers undergoing fetal surgery are at an increased risk for pulmonary oedema
Anaesthesia has traditionally been maintained with high concentrations of a volatile anaesthetic agent (1.5–2 MAC). Many centres use desflurane as the chosen agent for its rapid titratability. In 2010, Boat and colleagues reported the use of supplemental i.v. anaesthesia (SIVA) with propofol and remifentanil combined with lower concentrations of desflurane
Many centres are working to reduce the dose of volatile anaesthetic agents given to the mother, either by using SIVA, modifications of SIVA or other means (such as GTN infusions).
EXIT procedures
A fetal peripheral venous catheter or loop of umbilical cord close to the fetal abdominal cord insertion site may be used.
Fetal resus
support mother then support fetus
The fetus depends on uteroplacental support, and during fetal surgeries, preserving the uteroplacental circulation by maintaining maternal hemodynamics, achieving adequate uterine relaxation, preserving appropriate intrauterine fluid volume, and avoiding uterine contractions are critical
Fetal bradycardia is a reliable indicator of fetal compromise that must be addressed immediately
The common causes of fetal bradycardia include
- mechanical compression or kinking of the umbilical cord,
- uterine contractions,
- placental separation,
- maternal hypotension,
- umbilical artery vasospasm,
- anemia,
- hypoxemia.
Less common causes include
- fetal hypovolemia,
- hypothermia,
- anemia
All efforts to avoid maternal hypothermia should be used. The presence of placental circulation makes the fetal temperature highly dependent on maternal temperature, and maternal hypothermia will result in fetal hypothermia, which is associated with fetal bradycardia
Post-op
Indomethacin can cause constriction of the fetal ductus arteriosus. If administered for tocolysis, periodic fetal echocardiography monitoring should be performed to detect premature closure of the ductus arteriosus. This occurs most commonly at gestational ages <32 weeks.