Chapter 22: Fetal Considerations in the Critical Care Patient

Virtually any pathologic process which affects the mother has the potential to affect the fetus. The type and severity of the 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 the fetal physiology as it relates to these functions.

The fetal impact of most critical diseases in the mother will depend on how well the mother is able to continue to deliver oxygen to the fetus while at the same time dealing with her own compromised state. Fetal oxygen delivery depends on placental blood flow, differences in partial pressure of oxygen between mother and fetus, oxygen content (a function of oxygen carrying capacity of the maternal blood), the placental surface area, and is inversely proportional to the thickness of the placental diffusing membrane. In diseases that primarily affect the mother, except for those that may lead to abruptio placentae, placental issues remain constant and the critical issues become blood flow and oxygen pressure and content.

The fetus functions at a much lower oxygen tension than its air breathing counterpart. Its ability to do so is based on a hemoglobin/oxygen dissociation curve that is to the left of its mother (Fig. 22-1) allowing a considerably higher oxygen saturation at lower partial pressures of oxygen. This is absolutely essential in the human placental model which has a type of parallel flow that has been described as “concurrent." In this flow model (Fig. 22-2) the maximum fetal PO₂ will be a few torr 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, the fetal PO₂ can never exceed that of maternal venous blood. Thus, in the healthy, normally perfused placenta, fetal venous blood (the oxygenated side of the fetal circuit) will have a maximum PO₂ of about 35 given that mother’s venous PO₂ of 35 to 40. At this PO₂, the fetal blood is about 70% saturated with oxygen. The fetus will maintain aerobic metabolism at saturations above 30% to 35% corresponding to a PO₂ of 15 to 20. This is important information when trying to understand the impact of maternal hypoxia with alterations in uterine blood flow, such as with the mother with acute respiratory illnesses and especially with a mother on a ventilator. Maternal anemia will significantly alter the level at which anaerobic metabolism and acidosis may occur since reduced levels of hemoglobin will reduce the absolute amount of oxygen the blood will carry at a given saturation and PO₂. Conversely in the absence of maternal hypoxemia, the fetus may become hypoxic due to anemia alone at severely low levels. (Fig. 22-3) The exact level at which this may occur is not well known and is probably variable.

In other maternal critical care situations, blood flow will be the determinant 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 trimester, maternal cardiac output reaches its maximal level and peaks at about 6 L/min. Maternal blood volume is similarly increased. Approximately 750 cc/min of the maternal cardiac output flows through the low-resistance placental bed. Uteroplacental perfusion is critical to the maintenance of fetal oxygen and even minor alterations may result in fetal hypoxia. Several potential alterations may occur in the critically ill patient that can result in decreased placental perfusion. A large amount of occult 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 cc (30%) of maternal blood volume may be lost without significant changes in vital signs as opposed to only about 1000 cc (20%) in the nonpregnant female. The placental bed is neurologically linked to the maternal splanchnic bed and the physiologic response to decrease in blood volume in the mother is diversion of blood away from the placenta when other vital organs (brain, heart, adrenals) must be preserved. In such situations, the fetus may even become hypoxic even before shock occurs. Hypovolemia may result in decreased cardiac output further decreasing placental perfusion. While it may seem paradoxical, hypertension is also associated with decreased placental perfusion and the more severe the blood pressure elevation, the more likely one will face an underperfused placenta associated with fetal hypoxia. And finally, often critical situations result in the premature onset of contractions which further decrease uterine blood flow during the contractile epochs.

In almost all critically ill patients, as compared to immediate delivery of the compromised fetus, the better choice is to improve maternal condition in a way in which maternal benefit will result in improved fetal condition. While the fetus may often demonstrate signs of hypoxia as a result of the maternal compromise, the temptation to proceed with delivery can result in destabilization of the mother, unnecessary surgery (ie, cesarean section), and often the unnecessary delivery of a premature infant with 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 adequate maternal resuscitation.

There are some general elements that are common to evaluating and caring for the fetus when there is a critical illness in the mother. The first issue is to determine the gestational age and potential viability of the fetus. The approach to subsequent evaluation and management will always depend on this issue. To maximize fetal well-being in general, be sure the mother has some left uterine displacement usually best accomplished with a roll under the left buttocks. Administer oxygen by face mask using a tightly fitting nonrebreathing mask whenever possible. Determine as quickly as possible the general condition of the mother including especially her primary diagnosis, her vital signs, and hemodynamic status and include pulse oximetry to quickly determine her oxygen saturation. Maternal evaluation will include palpation of the uterus for size, fetal position, tenderness and contractions, and, where appropriate, may also include a perineal or even pelvic examination to assess for bleeding, rupture of membranes, and cervical dilation. At that point, if the fetus is of a viable gestational age, cardiotachometry is the critical next step. This modality will assist in determining the fetal oxygen status and uterine perfusion and whether there are contractions present. The ultrasound evaluation of the fetus should be reserved until the fetal well-being has been assured and contraction status has been determined. The level of detail required of the ultrasound will be determined by the preceding evaluations. Ultrasound will be important in being sure there is not an obvious lethal anomaly (eg, anencephaly) making the fetal evaluation moot. It may be important to confirm the gestational age and fetal viability to make the correct decision regarding timing and route of delivery. Ultrasound may be used as a tool to further evaluate fetal condition if the fetal heart rate (FHR) is not reassuring with biophysical profile including amniotic fluid volume assessment. And in some situations, more sophisticated fetal assessment such as Doppler flow studies may also become useful (Fig. 22-4).

Trauma

The leading cause of death and adverse outcome in the patient with major trauma is death of the mother. Thus the 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 and late decelerations may be the earliest sign of this problem even before major changes in maternal vital signs.

Evaluation for intra-abdominal hemorrhage may be more difficult because the enlarged uterus makes abdominal examination more difficult and the tenting of the peritoneum and anti-inflammatory effects of progesterone may dampen normal tenderness. Ultrasound can be useful in detecting intraperitoneal bleeding and open peritoneal lavage has been used with success in pregnancy. In the hemodynamically compromised patient who is tachycardic and hypotensive, aggressive fluid management is critical. In those patients, where in addition vasopressors are needed, care should be taken to consider the effects 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. Ephedrine may be considered as it is one agent known not to adversely affect uterine circulation.

The obstetric complications of major blunt trauma include abruptio placentae, fetal-maternal hemorrhage (with or without abruption), labor (and premature labor in the preterm gestation), and very 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 a tachysystolic contraction pattern and late decelerations (Fig. 22-5). Ultrasound will usually not reveal an acute abruption as the ultrasonic density of fresh bleeding is virtually identical to the placenta. Evaluation of the patient should also include laboratory assessment of hematocrit, fibrinogen, and platelet count for retroplacental consumptive coagulopathy, and a Kleihauer-Betke to rule out major fetal-maternal hemorrhage and determine whether and how much Rh-negative immune globulin is needed.

Delivery is generally the only option for patients with abruption. There is often a conflict, as the trauma team wants to be sure the mother has adequate diagnostic studies to rule out intracranial or other injuries. The obstetrician must become the advocate for the fetus and 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).

Rarely a patient will have a major fetal-maternal hemorrhage without a significant clinical abruption. Fetal heart rate findings may include tachycardia, decreased variability, late decelerations, and/or sinusoidal patterns. A biophysical profile may reveal a depressed fetus. Kleihauer-Betke will reveal the size of the fetal hemorrhage. Whether middle cerebral artery Doppler studies will be diagnostic in this situation is unknown at this time. In the very early gestation, emergency intrauterine transfusion can be an alternative to delivery.

Following the initial evaluation, there should be a more prolonged period of FHR and contraction monitoring (Fig. 22-6). The duration of monitoring will depend on the severity of the injury, presence of contractions and/or vaginal bleeding, and other clinical findings. Following any significant abdominal trauma, the fetus should be observed on the monitor for a minimum of 4 hours and if any signs of abruption exist for at least 24 hours (Fig. 22-7).

Hypoxia

Maternal hypoxemia may obviously lead to fetal hypoxia. Situations where acute hypoxia may present a challenge for fetal assessment and management may include an acute asthmatic episode, acute respiratory distress, often associated with sepsis (pyelonephritis, appendicitis), pulmonary edema with preeclampsia/eclampsia, cranial injuries with respiratory failure, amniotic fluid or pulmonary embolism, cardiac decompensation (eg, pulmonary edema associated with mitral stenosis), pneumonia, and irritant inhalation or burns.

Therapy is directed to the primary condition of the mother. Fetal heart rate monitoring will be useful in assessing how the fetus is tolerating any reduced oxygen delivery. In the absence of uterine contractions, a hypoxic fetus will develop tachycardia and loss of variability, and prolonged decelerations will only be seen preterminally. If contractions are present, late decelerations may be seen. A general goal for optimizing fetal oxygenation is to keep maternal PO₂ above 60 mm Hg and O₂ saturation above 90%. Levels below this on supplemental oxygen with rebreathing mask may require ventilator therapy. The goal should also be to avoid either hypercarbia or hypocarbia. The pregnant women normally hyperventilate and a PCO₂ of 35 is normal in pregnancy and lower levels may be associated with decreased placental perfusion. The goal should be maintaining PCO₂ between 35 and 40.

While colloid oncotic pressure may play a role in maintaining intravascular volume, and logically situations like pulmonary edema would be reduced with intravenous colloid administration, this should not be used in such situations, especially in acute situations. The problem is that the protein may leak into the pulmonary interstitium and further aggravate the ventilation perfusion mismatch. Severe anemia, however, should be corrected with packed red cells as maximizing oxygen carrying capacity is critical to fetal oxygen delivery.

Delivery is rarely indicated in situations of maternal respiratory failure unless the mother cannot be adequately oxygenated on full ventilatory settings. One other rare situation which may require delivery, especially in the third trimester is in the mother with a muscle weakness situation (eg, spinal muscular atrophy) where the elevation of the diaphragm compromises breathing and only delivery provides adequate relief.

Sickle Cell Crisis

While not truly a hypoxemic event, patients with sickle cell crises have compromised oxygen carrying capacity. Often patients who present with sickle cell crisis in the late second or third trimester will have fetal signs of hypoxia on the FHR monitor. Evaluation and management of the fetus will be virtually identical to patients with acute asthmatic episodes or other examples of respiratory failure. Thus, aggressive maternal therapy aimed at maximizing oxygenation and uterine perfusion is important. Rarely will intervention for fetal compromise be necessary. Blood transfusion may be more important for the fetus in such situations than for mother alone, as increasing oxygen carrying capacity improves fetal oxygen transfer. Improvement in the FHR should be expected as the crisis is resolving.

Anaphylaxis

Anaphylaxis is an acute allergic reaction with systemic manifestations that can include urticaria, respiratory distress, and cardiovascular collapse. The inciting agent may be food or medication.

With either respiratory compromise or shock or both, fetal hypoxia would be expected. The treatment is similar to the nonpregnant patient. Urgent resuscitation includes maintenance of an airway, oxygen administration, epinephrine, diphenhydramine, and intravenous hydration. The FHR may manifest late decelerations with or without tachycardia. Correction of maternal hypoxia and blood pressure should restore placental perfusion and correct the fetal hypoxia and the accompanying FHR pattern, although there may be a time lag of up to 2 hours before the FHR returns to complete normalcy.

Hypertensive Crisis

Acute hypertensive crisis in pregnancy may occur for reasons similar to those in the nonpregnant patient such as poorly controlled chronic hypertension, pheochromocytoma, or may occur as a result of severe preeclampsia/eclampsia. In either case, the principles of maternal therapy and the fetal considerations are similar. The blood pressure must be lowered to less dangerous levels to avoid severe secondary complications in the mother, principally intracranial hemorrhage. The obstetric benefit of lowering blood pressure at these high levels may also be to avoid abruptio placentae. However, acute reduction of the blood pressure must be done very carefully, as in these cases the fetus may not tolerate too large a drop in pressure, especially if accomplished too rapidly. This is true regardless of the agent used. The goal should be to lower pressure gradually over 30 to 60 minutes and to not reduce the pressure to normotensive levels. For example, the patient with an admission blood pressure of 220/130 mm Hg should be gradually reduced to a pressure of approximately 160 to 170/100 to 105 mm Hg. Medications such as apresoline, labetalol, or even nitroprusside may be used in either small boluses or by slow intravenous infusion as these drugs allow titration of blood pressure without overshooting if used appropriately.

In the case of the chronic hypertension, especially early in pregnancy, where delivery is not immediately planned, blood pressure should also be controlled with care not to overcorrect the levels. The fetus may demonstrate growth restriction or even hypoxia if blood pressure levels in severe hypertensives are overly corrected.

Maternal Acidosis

Rarely situations of maternal metabolic acidosis in the absence of hypoxemia or shock will present an extraordinary management challenge from a fetal perspective. Most commonly, this will be seen with diabetic ketoacidosis (DKA), but other situations such as drug- or toxin-induced acidosis (eg, aspirin overdose) may also present similarly. Generally speaking, the fetus will become acidotic slowly as buffers, including especially HCO3⁻, move slowly across the placenta from the fetal to the maternal intravascular compartment. This buffer depletion in the fetus then results in fetal acidosis. The fetus will demonstrate loss of variability with or without late decelerations on the FHR monitor and biophysical parameters including fetal movement, breathing, and tone will be reduced or absent. In such situation, maternal correction of the acidosis will improve the fetal condition and delivery is usually not warranted. The key point is that the fetal condition will require several hours or more beyond correction of the acidosis in the mother for its acidosis to clear as well (Fig. 22-8). Again the reason is that the fetal buffer must equilibrate back from the maternal to the fetal side of the placenta and because these are either very large or negatively charged buffers, this process occurs at a very slow rate. Continuous FHR monitoring during the correction of the maternal acidosis will provide information as to when the fetus is recovering. Rarely the fetus may deteriorate before the maternal acidosis can be corrected to the point of developing a preterminal prolonged deceleration/bradycardia. In this situation, if maternal condition permits and the fetus is of a viable gestational age, emergent cesarean section may be required.

In the situation of DKA, and perhaps in other such nonhypoxic metabolic acidoses, the mother will be severely dehydrated as well. This may result in underperfusion of the placenta and hypoxia may compound the metabolic acidosis. Therefore, it is equally important to correct the dehydration with aggressive fluid administration.

Seizures

Maternal seizures, whether due to eclampsia, epilepsy, or even metabolic disturbances, will usually result in major alterations in the parameters used to assess fetal well-being, especially the FHR. Seizures may alter placental perfusion and hence fetal oxygenation in several ways. Maternal hypoxia often results from suspended breathing. Diversion of blood flow away from the uterus will occur because of the intense maternal muscular activity. And finally, probably as result of the intense uterine ischemia, there will often be tetanic or prolonged uterine contractions occurring during the seizure. All of these factors together will most often result in the anticipated changes in the FHR. Usually a prolonged deceleration or deep late decelerations will occur during the seizure. Once the seizure resolves, the deceleration(s) will resolve, but a period of tachycardia and reduced FHR variability will occur, often lasting 30 minutes to 2 hours. If the FHR was normal preceding these changes and the mother is now well oxygenated and seizure free, the FHR will gradually return to normal (Fig. 22-9).

Therapy is directed at maternal condition. The keys as with nonpregnant patients are to maintain the airway, and avoid maternal injury. Tilting the mother to her left side will avoid aortocaval compression. Once the seizure is resolved, treatment is aimed at preventing further seizures with medication and then treating the cause when possible. The choice of medications for treatment of acute seizures, or with status epilepticus, must be made with the fetus in mind. Azodiazepams should be used cautiously if there is a chance the baby will need to be delivered, especially if the fetus is premature, as these drugs alter thermoregulation and are neurodepressive. In such cases short-acting barbiturates (eg, pentobarbital) are reasonable alternatives. Delivery is rarely needed for the FHR changes due to the seizure and, in most situations, it is better to allow the placenta to resuscitate the fetus even if immediate delivery is warranted, such as with eclampsia.

Thyrotoxicosis

Acute thyrotoxicosis and, especially, thyroid storm are obstetric emergencies that have significant fetal implications. Potential complications include asphyxia, premature labor, preeclampsia, and fetal hyperthyroidism. The mechanisms of the potential fetal compromise are multifactorial. The maternal hyperdynamic state will divert blood flow away from the uterus. Uterine ischemia may lead to intrauterine growth restriction (IUGR), fetal hypoxia, and/or premature contractions. Superimposed preeclampsia may further aggravate the placental hypoperfusion. Thyroid immunoglobulin is an IgG and crosses the placenta potentially causing fetal hyperthyroidism increasing metabolic demands of the fetus. With thyroid storm, besides being a more intense hyperdynamic state amplifying the potential fetal compromise, there may also be maternal heart failure and pulmonary edema superimposing maternal hypoxemia.

The FHR may be altered in any number of ways depending on which of these complex factors are involved at any one time. Tachycardia may be either due to the maternal disease or fetal hyperthyroidism. Late decelerations may occur if placental hypoperfusion is severe. Treatment, as with other similar situations where correction of maternal condition will usually improve fetal condition, thus does not require immediate delivery.

Cardiac Arrest

The presence of an enlarged uterus, especially with a gestational age more than 24 weeks, compromises the ability to resuscitate the mother when cardiac arrest occurs. This is primarily due to aortocaval compression but is also aggravated by the blood flow going to the low-resistance uteroplacental bed which is critically needed by the vital organs of the mother. Furthermore, the potential for fetal asphyxia in the case of maternal cardiac arrest is very high.

Cardiopulmonary resuscitation in the pregnant woman, thus involves 2 principal differences. The first is to assure left uterine displacement. Tilting the maternal trunk may not be the best option as this may compromise the efficiency of chest compression. It is recommended that either the entire backboard be tilted or that an assistant manually displaces the uterus to the left. The second issue is the timing of the delivery. Katz et al performed a large review of cardiopulmonary arrest in pregnancy. Fetuses delivered within 5 minutes of maternal death all survived and appeared to be neurologically intact. Given this information and the knowledge that the pregnancy compromises the resuscitation, it is recommended that bedside cesarean section be begun if the resuscitation has not restored cardiac function within 4 minutes, so as to accomplish delivery within 5 minutes.

Brain Death and Life Support

A few cases of prolongation of pregnancy in an effort to reach a viable or near-mature gestation have been reported in the mother who is brain dead but remains on cardiopulmonary life support. In these cases delivery was required for sepsis, fetal distress, or maternal hypotension. Thus, it is critical to use continuous fetal monitoring once viability is reached, maintain adequate uteroplacental perfusion with aggressive hemodynamic monitoring and fluid management, and avoid infection. Tocolysis can be considered as needed. Setup at bedside for immediate cesarean section should be available at all times.

SUMMARY

The principles of fetal evaluation and management for maternal critical care situations are remarkably similar for most conditions. Correction of the maternal condition and/or stabilization of maternal cardiorespiratory status should always be the first goal. Whenever possible, if the condition can be reversed, the ultimate goal should be to correct the maternal condition without the necessity for premature delivery. If delivery will improve the maternal condition, as in severe preeclampsia/eclampsia, the mother should still be stabilized before delivery should occur. A thorough understanding of the physiologic changes in pregnancy, how these affect maternal evaluation, and how pathologic condition affects fetal oxygen delivery and uteroplacental perfusion are the critical steps in understanding the fetal component of evaluation and management of the critical care pregnant patient.