Virtually any pathologic process which affects the mother has the potential to affect the fetus. The type and severity of fetal impact will depend on many variables among which are whether the insult is acute or chronic, how the insult affects fetal oxygenation via oxygen delivery and uterine perfusion, and the ability to intervene based on gestational age and the hemodynamic and respiratory status of the mother. Critical to decision making in these situations is a basic understanding of fetal physiology as it relates to these functions.

The fetal impact of most critical maternal diseases depends on how well the mother is able to deliver oxygen to the fetus while simultaneously dealing with her own compromised state. Fetal oxygen delivery depends on adequacy of placental blood flow, sufficient differences between fetal and maternal partial pressures of oxygen, sufficient oxygen content (a function of oxygen carrying capacity of the maternal blood), and adequacy of placental surface area. Fetal oxygen delivery is inversely proportional to the thickness of the placental diffusing membrane. Except for maternal diseases that may lead to abruptio placentae, placental issues are generally static in critical care situations. Thus, critical factors which influence fetal well-being in critical care situations are essentially uteroplacental blood flow and maternal oxygen pressure/content.

Fetal red blood cells possess hemoglobin F, a form of hemoglobin which binds more avidly to oxygen than does (maternal) hemoglobin A. Therefore, the fetus thrives at much lower oxygen tensions than can its mother. Its ability to do so is based on a hemoglobin/oxygen dissociation curve that is shifted to the left of its mother’s as a result of its hemoglobin F (Fig. 22-1), thereby producing considerably higher oxygen saturations at lower partial pressures of oxygen. This is essential in the human placental, which has a parallel flow arrangement, usually described as “concurrent.” In this model (Fig. 22-2), the maximum fetal PO₂ will be a few torr (mm Hg) less than that of the mother’s venous PO₂. This is because at the end of the exchange loop, for oxygen to be continually exchanged in the direction of mother to fetus, fetal PO₂ can never equal or exceed that of maternal venous blood. Thus, in healthy, normally perfused placentas, fetal venous blood (the oxygenated side of the fetal circuit) will have maximum PO₂ values of about 35 torr, versus maternal venous PO₂ ­values of 35 to 40 torr. At this PO₂, the fetal blood will be roughly 70% saturated with oxygen. The fetus will maintain aerobic metabolism at saturations above 30% to 35% corresponding to a PO₂ of 15 to 20 torr. This is important information when trying to understand the impact of maternal hypoxia with concomitant alterations in uterine blood flow, such as the mother with acute respiratory illnesses, especially one requiring a ventilator. Additionally, maternal anemia may significantly alter the level at which anaerobic metabolism and acidosis occur, since reduced levels of hemoglobin will reduce the absolute amount of oxygen the blood will carry at a given saturation and PO₂. In the absence of maternal hypoxemia, the fetus may become hypoxic in the setting of severe anemia alone (Fig. 22-3). The exact level at which this may occur is not well known, but likely variable.

In other critical maternal situations, blood flow will be the final arbiter of whether adequate fetal oxygenation is occurring. Uterine blood flow is generally a function of maternal cardiac output. Normally during the late second and early third trimesters, maternal cardiac output reaches its maximal level; peaking at about 6 L/min. Maternal blood volume is similarly increased. Approximately 750 mL/min (about 10%-20%) of maternal cardiac output flows through the low-resistance placental bed. Uteroplacental perfusion is critical to the maintenance of fetal oxygen levels; even minor alterations may result in fetal hypoxemia and hypoxia. For example, a large amount of occult maternal blood loss (eg, intraperitoneal) may not be as readily apparent in pregnancy because of the marked increase in blood volume and the ability of the mother to redistribute blood away from the uterus. As much as 2000 mL (30%) of maternal blood volume may be lost without significant changes in vital signs, as opposed to only about 1000 mL (20%) in the nonpregnant female. The placental bed is neurologically linked to the maternal splanchnic bed; the physiologic response to decrease in maternal blood volume is diversion of blood away from the placenta while blood flow to other vital organs (brain, heart, adrenals) is preferentially preserved. In such situations, the fetus may become hypoxic even before maternal shock occurs. Hypovolemia may result in decreased cardiac output, further decreasing placental perfusion. While seemingly paradoxical, hypertension is also associated with decreased placental perfusion. Indeed, the more severe the blood pressure elevation, the more likely underperfusion of the placenta will occur, with consequent fetal hypoxia. Critical situations not infrequently result in premature onset of contractions, which further decrease uterine blood flow during uterine systole. Other maternal physiologic changes to be considered when evaluating mother and fetus in critical care situations include reduced pulmonary functional residual capacity and increased oxygen consumption which together may lead to rapid development of maternal hypoxemia, particularly if the mother becomes apneic or is otherwise hypoventilating. Also, pregnancy-associated increases in maternal levels of progesterone decrease gastrointestinal motility. In such situations, the mother is more likely to aspirate stomach contents, especially if obtunded or anesthetized, thereby leading to further hypoxemia and hypoxia.

In almost all critically ill patients, as opposed to immediate delivery of a compromised fetus, the better choice is to improve maternal status, which will result in improved fetal physiologic status. While the fetus may often demonstrate signs of hypoxia as a result of maternal compromise, the well-intentioned urge to proceed with delivery may result in destabilization of the mother, unnecessary surgery (ie, cesarean delivery), and (often) unnecessary delivery of a premature infant who exhibits the inherent complications of prematurity. One glaring exception to this is in the case of cardiopulmonary arrest, where delivery of the fetus may be the only way to allow successful maternal resuscitation.

There are some general considerations common to evaluating and caring for the fetus when the mother is critically ill. The first issue is to determine the gestational age of the fetus. To optimize general fetal well-being, ensure that the mother is receiving left uterine displacement, usually best accomplished with a roll or wedge under her right buttocks. Administer oxygen by face mask using a tight-fitting non-rebreather mask, whenever possible. Quickly determine general condition of the mother, including her primary diagnosis, vital signs, and hemodynamic status; include pulse oximetry to quickly estimate her oxygenation status. Maternal examination will include palpation of uterine size, fetal position, presence of tenderness and/or contractions. Where appropriate, include a perineal and pelvic examination to assess for bleeding, rupture of membranes, and degree of cervical dilation. At this point, if the fetus is of viable gestational age, cardiotachometry is critical. This modality will assist in determining the status of fetal oxygenation and uterine perfusion, as well as whether contractions are present. Ultrasound evaluation of the fetus should be reserved until fetal well-being has been assured and contraction status has been determined. The level of sonographic detail required will be determined by the preceding evaluations. Ultrasound will be important to rule-out obvious lethal anomalies (eg, anencephaly) which would render further fetal evaluation moot. It may be important to confirm the gestational age and fetal presentation so as to make the correct decision regarding timing and route of delivery. Ultrasound may be used as a tool to further evaluate fetal condition via biophysical profile assessment(s) if the fetal heart rate (FHR) is not reassuring. In some situations, more sophisticated fetal assessment such as various Doppler-flow studies may prove useful (Fig. 22-4).

Trauma

The leading cause of fetal death and severe sequelae is death of the mother. Thus, initial evaluation and management, other than the steps outlined in the previous section, will be to ensure that the mother is appropriately assessed and stabilized. Major hemorrhage in the mother may lead to decreased placental perfusion and fetal hypoxia, and must be controlled. Occult intra-abdominal hemorrhage may lead to diversion of blood away from the uterus; late decelerations may be the earliest sign of this problem, even before major changes in maternal vital signs develop. Moreover, intra-abdominal hemorrhage may be more difficult to assess because the enlarged uterus makes abdominal examination challenging. Tenting of the peritoneum and anti-inflammatory effects of progesterone may dampen the ability to assess tenderness. Ultrasound may detect as little as 200 mL of intraperitoneal blood, although open peritoneal lavage has historically been successfully used in pregnancy. In the hemodynamically compromised patient who is tachycardic and hypotensive, aggressive fluid management is critical. In those patients, where in addition of vasopressors is needed, care should be taken to consider the effects of the pressors on the fetus. Low-dose dopamine, which in the mother is effective primarily due to increased cardiac output, has been shown in animals to decrease uterine perfusion, so careful fetal monitoring is warranted. Norepinephrine and isoproterenol may have similar fetal effects. However, ephedrine is known to not adversely affect uterine circulation.

The obstetric complications of major blunt trauma include spontaneous abortion, stillbirth, abruptio placentae, fetal-maternal hemorrhage (with or without abruption), labor (term and preterm), and rarely, uterine rupture and fetal trauma. In patients without obvious clinical abruption (ie, uterine contractions, pain, tenderness, and vaginal bleeding) the FHR monitor may be the most sensitive tool to detect abruptio placentae. The characteristic findings in abruptio placentae include tachysystolic uterine contraction patterns and FHR decelerations, both late and variable (Fig. 22-5). Ultrasound will usually not reveal an acute abruption, as the ultrasonic density of fresh bleeding is virtually identical to that of the placenta. Studies suggest that ultrasound in this situation has a sensitivity for identifying abruption no higher than 25%. Evaluation of the patient should also include laboratory assessment of hematocrit, fibrinogen, and platelet count for retroplacental consumptive coagulopathy. A Kleihauer-­Betke test should be performed to rule out major fetal-maternal hemorrhage and to determine whether and how much Rh-negative immune globulin is needed, should the mother have Rh negative blood.

Delivery is generally the only option for patients with severe abruption. On occasion, there may be conflict between well-intended care providers. For example, the trauma team may want to ensure that the mother has adequate diagnostic studies to rule-out intracranial hemorrhage or other serious injuries. The obstetrician must become the advocate for the fetus; open communication is essential. Tocolysis for premature labor associated with trauma-induced abruption should be approached with extreme caution. If considered at all, it should be limited to patients with very early gestational ages (ie, <32 weeks) and in those who are hemodynamically stable with reassuring fetal status, no active bleeding, and no coagulopathy. Corticosteroids for lung maturity should be used concurrently (Table 22-1).