A 35-year-old Gravida 1 Para 0 woman was admitted at 26 weeks and 6 days’ gestation for inpatient surveillance in the setting of decreased fetal movement and category II tracing. The patient’s medical history was notable for history of Roux-en-Y gastric bypass, a body mass index of 50 mg/k2, obstructive sleep apnea treated with nighttime continuous positive airway pressure, anxiety, depression, and gestational thrombocytopenia. The pregnancy course was otherwise benign.On arrival, the nonstress test was nonreactive despite vibroacoustic stimulation. The result of the biophysical profile was 6/10. There were periods of electronic fetal monitoring that had minimal variability with some characteristics of a sinusoidal pattern but not the “classic” pattern (Figure 1). Given the clinical picture, a fetal maternal hemorrhage was suspected, and laboratory and fetal evaluation was pursued. Results included a Kleibauer-Betke (KB) corresponding to more than 80 mL of fetal blood with normal maternal fibrinogen level, hematocrit, and platelet count. Fetal ultrasonography demonstrated a middle cerebral artery (MCA) Doppler that was elevated at 1.9 multiples of the median (MoMs) (Figure 2). The patient was counseled on the need for continuous electronic fetal monitoring and high concern for fetomaternal hemorrhage (FMH). A course of betamethasone was administered, and consent was obtained for possible cesarean delivery.The findings in this patient were suggestive of a clinically significant FMH given the KB corresponding to more than 80 mL, elevated MCA Doppler, and concerning fetal heart rate pattern. For this patient, given the early gestational age, the initial plan was to monitor the fetal heart rate continuously and provide betamethasone for fetal benefit. Multidisciplinary care with obstetrics, maternal-fetal medicine, and neonatology was coordinated. In preparation for possible delivery, leukoreduced blood was made available for the neonate. The fetal tracing was evaluated multiple times over the course of the day with progression to periods of sinusoidal tracing predominating over the age-appropriate pattern. An intrauterine transfusion was considered but not attempted given the concern for fetal coagulopathy with the large estimated FMH and potential limited benefit with an ongoing hemorrhage. Preparations were made for delivery; magnesium sulfate was initiated for fetal neuroprotection.Given the deteriorating fetal tracing and high concern for significant FMH, the patient was urgently transferred to the operating room to proceed with delivery via primary low transverse cesarean delivery approximately 12 hours after presentation.The cesarean delivery was uncomplicated. The patient received multiple doses of Rh immunoglobulin to cover the 80 mL fetal blood in her circulation.A viable female infant was delivered in the breech position. The umbilical cord was immediately clamped, and the infant was passed to awaiting neonatal intensive care unit personnel for further evaluation and management. The infant had an Apgar score of 3 and 8 at 1 and 5 minutes of age, respectively. The infant’s birthweight was 970 g.The neonate required intubation soon after birth and escalation in respiratory support over the course of her hospitalization. The infant’s initial hemoglobin was less than 3 g/dL and required mass transfusion of packed red blood cells, platelets, fresh frozen plasma, and cryoprecipitate. The infant’s severe anemia resulted in injury to the liver (transaminitis, coagulopathy, and liver hematoma) and kidneys (anuria, hyperkalemia, and acute kidney injury). Intraparenchymal and intraventricular hemorrhages were documented on head ultrasonography at 1 day after birth (Figure 3). A liver hematoma was also appreciated (Figure 4). The infant’s hypotension and lactic acidosis/metabolic acidosis progressed despite maximal medical therapy. The family ultimately decided to transition to comfort care given the deteriorating status despite extensive supportive measures at 3 days of age.The differential for decreased fetal movement is broad and includes severe fetal anemia, severe uteroplacental insufficiency, fetal sleep cycle, fetal anomalies, placenta cord abnormalities (eg, thrombosed cord), and fetal motor or neurological impairment.1 If a pregnant person presents with decreased fetal movements, fetal assessment with either a nonstress test or biophysical profile is advised. Delivery may be indicated pending results of fetal assessment. However, most commonly when someone presents with decreased fetal movement it is transient and not associated with pathophysiology.Decreased fetal movement has been associated with 2.9–4.5 increased odds of stillbirth.2 In a retrospective study of 203 pregnant patients who presented to an obstetric emergency service with decreased fetal movement, there were significant increased odds of small for gestation age (odds ratio OR, 19.5) and recurrence of decreased fetal movement was associated with poor perinatal outcomes (OR, 2.9).3The most common sign of FMH is decreased fetal movement.4 Abnormal fetal heart rate tracing (ie, bradycardia, tachycardia, loss of variability, and late decelerations) is present less than 10% of the time, and the classic sinusoidal pattern is rare. In the appropriate clinical scenario, when a pregnant patient presents with decreased fetal movement, the differential diagnosis includes an FMH and the evaluation may include a KB test or fetal MCA Dopplers.4FMH refers to fetal blood entering the circulation of the pregnant person.4 Minor bidirectional flow of blood between the fetus and pregnant individual occurs in a typical pregnancy.5 A disruption of trophoblasts allows fetal erythrocytes to enter the intervillous space and then into the circulation of the pregnant person.4 More than 80% of FMHs are idiopathic with no preceding event. Therefore, FMH is likely underreported and underrecognized.4 FMH is associated with fetal conditions including anomalies and multiple gestation.5 Other associations include placenta previa, abruption, and placental tumors, as well as trauma to the pregnant individual.5 Placental pathology associated with a FMH may demonstrate parenchymal pallor and elevated nucleated red blood cells.4The incidence of FMH greater than 30 mL is estimated to be 0.9–3/1000 births.4 The severity is related to the rate and to the volume of fetal blood loss. A KB test assesses quantitative amount of fetal blood in the circulation of the pregnant person and is a key means of evaluating the severity of the FMH. The KB test estimates the volume of Rh immunoglobulin necessary to protect against sensitization in the pregnant person of fetal Rh-positive blood in a Rh-negative pregnant patient. MCA Dopplers can also be used to aid in diagnosis, and more than 1.5 MoMs is suggestive of fetal anemia, although this does carry a false-positive rare of 12%.6 MCA Dopplers are elevated because cardiac output is increased to preferentially drive oxygenated blood to the fetal brain in periods of severe anemia. Measurement of the MoM is a way to compare a value against a normal median value for that specific gestational age.7If there is a high concern for clinically significant FMH at a preterm gestational age, preparation for a preterm delivery may be warranted with consideration of a betamethasone course depending on the individual clinical circumstances. In select cases, cordocentesis and intrauterine transfusion may be indicated.4,6 The use of intrauterine transfusion needs to be evaluated against the procedural risks including preterm premature rupture of membranes, abruption, preterm labor, bleeding in the fetus or pregnant person, worsening alloimmunization, and fetal death.6 Multidisciplinary care with the neonatology team and the blood bank to prepare for delivery and caring for potential sequela of significant hemorrhage is importantSmall FMHs are commonly tolerated by the fetus, but large untreated bleeds can lead to fetal cardiac failure, hydrops, hypovolemic shock, neurological injury, stillbirth, and neonatal death.4 Fetal mortality rates are 8 to 38%.5 This case of severe FMH at a preterm gestational age demonstrates that although many FMHs may be clinically insignificant, a minority may lead to terminal neonatal outcomes despite extensive medical intervention. The pathophysiology of this condition is not well known, and the current diagnostic criteria do not allow knowledge of timing of the bleed. Future research is needed to help fill gaps in pathophysiology, presentation, evolution, and safe management of substantive fetal hemorrhage.4American Board of Pediatrics Neonatal-Perinatal Content SpecificationKnow maternal medical disorders and medications affecting the fetus and newborn infant.Recognize abnormalities of the umbilical cord, fetal membranes, and placenta.
Todhunter et al. (Sun,) studied this question.