Acta Obstet Gynecol Scand 2003: 82: 479–480 Copyright C Acta Obstet Gynecol Scand 2003

Printed in Denmark . All rights reservedActa Obstetricia et

Gynecologica ScandinavicaISSN 0001-6349

CASE REPORT

Acute massive fetomaternalhemorrhage: case reports andreview of the literature

ANNIE THOMAS, MARIAM MATHEW, EVELYN UNCIANO MORAL

AND VLASTA VACLAVINKOVA

From the Department of Obstetrics and Gynecology, SultanQaboos University Hospital, Al Khod, Sultanate of Oman

Acta Obstet Gynecol Scand 2003; 82: 479–480. C Acta Obstet GynecolScand 82 (2003)Keywords: massive fetomaternal hemorrhage; fetal outcomeSubmitted 18 March, 2002Accepted 27 May, 2002

Massive fetomaternal hemorrhage occurs in approximately onein 1000 deliveries. For the majority the cause is unexplained.The warning sign is decreased fetal movements associated withabnormal cardiotocographic findings, such as decreasedvariability and a sinusoidal pattern, especially in a low riskpregnancy. We report two cases of acute massive fetomaternalhemorrhage in women with low risk pregnancies who presentedwith decreased fetal movements. The cardiotocograph showedreduced beat-to-beat variability in one case and a sinusoidalpattern in the other case. Both patients were delivered byemergency cesarean section and the newborns were profoundlyanemic. One baby died 12h after birth whereas the othernewborn had a good outcome.

Case 1

A 29-year-old primigravida had been regularly attending theantenatal clinic at SQUH. She presented with no risk factorswhen booking but later developed polyhydramnios. She wasadmitted at 36weeks of gestation with history of decreased fetalmovements since the previous night. The day before, she hadattended the antenatal clinic for her regular check up and thefetus was clinically and ultrasonically normal according to aDoppler flow velocimetry of the umbilical artery. The amnioticfluid index was 180mm.

On admission the cardiotocograph recorded poor beat-to-beat variability and there were no accelerations (Fig.1). Acouple of hours later, the trace recorded persistent bradycardiadown to 80 beats per minute without recovery, and hence thepatient had an emergency caesarean section under spinal anes-thesia. She was delivered of a male baby weighing 3300g withan Apgar of 1 at birth. The baby was resuscitated for 12min,was intubated and then transferred to the neonatal unit. Thecord pH was 6.7 and the hemoglobin level was 22.2g/l with ahematocrit of 7.2%. No reticulocytes or erythroblasts were seenon the peripheral smear and there was no evidence of hemo-lysis. The pH at 2h of birth was 6.92 with a base deficit of 23.The baby failed to maintain a satisfactory pH despite intra-

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venous fluids and a blood transfusion and succumbed at 12hof birth.

An autopsy showed a macroscopically normal fetus. Therewas a seriously negligible amount of fluid in the pericardialand pleural cavities, and was probably transudate. Histologyperformed on the bone marrow showed erythroid hyperplasia.There was extensive extramedullary hemopoesis in the liver andspleen. The Betke-Kleihauer test showed a massive fetomater-nal hemorrhage equivalent to 160ml. The mother had a hemo-globin of 126g/l and a hematocrit of 0.388 before the deliveryand her hemoglobin 2days postpartum was 140g/l with ahematocrit of 0.413.

The postpartum period for the patient was uneventful.

Case 2

A 28-year-old gravida 5, para 3 with history of three normaldeliveries and one abortion presented to the delivery suite atSQUH at 38weeks of gestation with history of absent fetalmovements for 10h before admission. She gave a history ofreduced fetal movements for the past 5days and had attendedthe accident and emergency department 48h before admission.As the nonstress test was reactive with good fetal movementsshe had been discharged home with a fetal kick count chart.Her pregnancy had so far been uneventful. Her blood groupwas O Rh-ve and the antibody screen was negative. The physi-cal examination on admission was unremarkable. The cardioto-cograph showed a sinusoidal pattern (case 2 in Fig.1). An ultra-sound scan did not show any fetal body or limb movements.The amniotic fluid index was 150mm. The sinusoidal patternwas followed by a prolonged bradycardia down to 90 beats perminute. She was delivered immediately by a lower segmentcesarean section under general anesthesia. The male newborn

Fig.1. Cardiographs of two patients with acute fetomaternalhemorrhage.

480 A. Thomas et al.

weighed 3200g, was extremely pale and hypotonic at birth, andhad an Apgar score of 1 at 1 min and 3 at 5min. The baby wasresuscitated, intubated and then transferred to the neonatalunit. The cord pH was 7.26 and the hemoglobin level was 30g/l. Fifty minutes after the birth, the patient’s arterial bloodshowed a pH of 7.12 and a base deficit of 16.3. The baby im-proved dramatically with the transfusion and was extubated 24h after birth. A three-packed cell transfusion of 15ml/kg eachraised the hemoglobin level to 136g/l. The Betke-Kleihauer testshowed a fetomaternal hemorrhage of 80ml, which was 30% ofthe neonate’s blood volume. On admission the mother’s hemo-globin was 98g/l with a hematocrit of 0.332. In spite of a bloodloss of 1000ml during the caesarean section, the post operativehemoglobin was 96g/l and the hematocrit was 0.335. The postpartum period was uneventful.

Discussion

Massive fetomaternal hemorrhage (FMH), though uncommon,is not rare. In one series, hemorrhages of 80ml or greater oc-curred in one of 1146 pregnancies screened routinely at delivery(1). There are several possible causes of fetomaternal hemor-rhage such as placental abruption, maternal trauma or pro-cedures such as external cephalic version or amniocentesis. InGiacoia’s study the cause was not identified in 82% of the cases(2).

Women who usually present with reduced fetal movementshave cardiotocographic abnormalities like reduced variabilityor sinusoidal rhythm. The fetal outcome depends on theamount and rate of bleeding. In a published review the outcomeranged from one asymptomatic newborn who bled 435ml, re-presenting more than his total fetoplacental blood volume, to aseverely ill newborn with poor outcome who bled 80ml, repre-senting 20% of his blood volume (1). The authors summarizedthat in these two cases, the rate of bleeding was an importantfactor in their differing outcomes. In acute FMH, rapid bloodloss is followed by perinatal hypoxia and intrauterine death orsevere anemia and hypoxia at birth.

In chronic cases, the fetus reacts by compensatory mechan-isms of increased hemopoetic activity revealed by increasederythroblasts and reticulocytes in the peripheral smear (2). In-adequate compensatory reaction will lead to development ofhydrops (3). Often the diagnosis is postnatal. If diagnosed ante-natally, in preterm patients it can be treated with an intra-uterine blood transfusion if the facility is available.

Kosasa et al. have described three cases with decreased orabsent fetal movements and the cardiotocograph showed absentvariability and deceleration. Immediate caesarean deliverieswere performed. All three infants were severely anemic but thehemoglobin levels were between 53g/l and 65g/l. All three ba-bies survived (4). In our Case 1, the hemoglobin was 22g/l; mostprobably the lowest reported in literature for acute hemorrhage.Classically fetal anemia presents with a sinusoidal pattern onthe cardiotocograph, as in our Case 2. These cardiotocographicabnormalities are late signs and usually associated with poorfetal outcome (2,3,5). A subtle sign of fetomaternal hemorrhagecould be an increase in maternal hematocrit (4). In both ourcases there was a rise in the maternal hemoglobin.

The Betke-Kleihauer test should be performed in patientspresenting with decreased fetal movements and with either ofthese FHR abnormalities, especially when the pregnancy had

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no known risk factors. The Betke-Kleihauer test is dependenton the fact that adult hemoglobin is more readily elutedthrough the cell membrane in the presence of acid than is fetalhemoglobin. The maternal blood is fixed on a slide with ethanol(80%) and treated with citrate phosphate buffer to remove theadult hemoglobin. After staining with hematoxylin and eosin,the fetal cells can readily be distinguished from the empty mat-ernal cells. All cells are counted, and an estimate of the extentof the fetal to maternal hemorrhage (measured in ml) is madebased on the following equation:

No. of fetal cells counted

No. of maternal cells counted

Ωestimated fetal blood volume (ml)

estimated maternal blood volume (ml)

The diagnosis of fetomaternal hemorrhage should be con-sidered in all cases of unexplained fetal death, fetal distress,nonimmune hydrops fetalis, neonatal shock and nonhemolyticneonatal anemia. The prognosis in cases of fetomaternalhemorrhage is poor and may be improved by prompt deliveryand a neonatal transfusion, or if the fetus is premature by cordsampling and an intrauterine transfusion (6,7).

References

1. de Almeida V, Bowman JM. Massive fetomaternal hemor-rhage: Manitoba experience: Obstet Gynaecol 1994; 83:323–8.

2. Giacoia GP. Severe fetomaternal hemorrhage: a review. JObstet Gynecol Surv: 1997; 52 (6): 372–380.

3. Elliot JP. Massive fetomaternal hemorrhage treated by fetalintravascular. Transfusion Obstet Gynaecol 1991; 78: 520–3.

4. Kosasa TS, Ebasugawa I, Nakayama RT, Hale RW. Mass-ive fetomaternal hemorrhage preceded by decreased fetalmovement and a nonreactive fetal heart rate pattern. Ob-stet Gynaecol 1993; 82 (4): 711–14.

5. Tsuda H, Matsumoto Sutoh Y, Hidaka A, Imanaka M,Miyazaki A. Case report. Massive fetomaternal hemor-rhage. Int J Gynecol Obstet 1995; 50: 47–9.

6. Fischer RL, Kuhlman K, Grover J, Montgomery O, WalperWJ. Chronic, massive. fetomaternal hemorrhage treatedwith repeated fetal intravascular transfusions. Am J ObstetGynaecol 1990; 162: 203–4.

7. Rouse D, Weiner C. Ongoing fetomaternal hemorrhagetreated by serial fetal. intravascular transfusions. ObstetGynaecol 1990; 76: 974–5.

Address for correspondence:Annie ThomasSenior RegistrarDepartment of Obstetrics and GynecologyCollege of MedicineSultan Qaboos UniversityPO Box 35Code 123Al Khod Sultanate of Omane-mail: anntho61/hotmail.com