A Case Report of Placental Infarction Department of Pathology, Kurume

THE KURUME MEDICAL JOURNAL Vol. 28, p. 137-140, 1981

A Case Report of Placental Infarction

DAIJI SATO, YASUYUKI SHINOHARA, AKIHIKO NAKASHIMA, YOSHIAKI HOSOKAWA, TERUYUKI NAKASHIMA AND NOBU IDE Department of Pathology, Kurume University School of Medicine and *St . Mary's Hospital, Kurume, 830 Japan

Received for publication April 7, 1981

Summary: A 31-year-old Japanese female, gravida 4, para 0, who had previously experienced three spontaneous abortions during 7 th or 8 th month of gestation was diagnosed with intrauterine fetal death at 26th weeks of gestational age. Investigations for maternal and fetal etiologies, including toxemia, incompatibility of blood groups and types, and infections, proved negative. Anoxia which resulted in the demise of the fetus is believed to have been responsible for the rare combination of extensive placental infarction in an asymptomatic gravid woman.

Key words: placenta•\placental infarction•\infarction•\fetal death•\ intrauterine fetal death

Introduction The third fetus was autopsied, but the cause of fetal death could not be determi- Placental infarction is not a rare lesion. ned. Extensive placental infarction leading to The patient's last menstrual period was intrauterine fetal death is a not uncom- June 15, 1980. This patient was closely mon complication of toxemia (preeclamp- observed as a high risk pregnancy. When sia), antepartum hemorrhage, and chronic examined at 15 weeks of gestation, the renal disease. Extensive placental infarc- patient's weight gain was less than normal tion without maternal complication, how- and the height of fundus uteri was observed ever, is very rare. Fox (1967) described to be lower than normal for 15 th weeks only one case of extensive placental infarc- of gestation. She was consequently admit- tion in 15 cases of unexplained intrauter- ted to St. Mary's hospital for maintenance ine fetal death with uncomplicated preg- of graviditas. nancies. We report a case of diffuse and Laboratory data included hemoglobin large infarctions of placenta without ma- level 15.1g/dl, hematocrit 42.5%, leuko- ternal complications that resulted in the cyte count 7700, and erythrocyte count demise of the fetus. 453•~104, total protein 7.3g/dl, albumin 3.5g/dl, blood urea nitrogen 11mg/dl, creatinine 0.8mg/dl, and cholesterol 209 Case mg/dl. Other data for liver function revealed normal levels. Urinary estriol (E3) A 31-year-old Japanese female, gravida was 5mg/day, HPL 1.2ƒÊg/ml, HsALP 4, para 0, had previously experienced three 2.9U., and HsLAP 116U. The antibody spontaneous abortions during the 7 th or titer for Toxoplasma was less than 16x, 8 th month of gestation from 1976 to 1979. Herpes simplex 64x, Cytomegalovirus 32x,

137 138 SATO, ET AL.

Rubella 64x, and Wassermann's reaction among the chorionic villi. In the former was negative. Incompatibility testing of lesion severe leukocytic infiltration was blood groups and types proved negative. observed in the decidua and intervillous At 26th weeks of gestational age, the spaces. Pooling of erythrocytes and deposi- fetus was spontaneously aborted. The fetus was then autopsied.

Pathologic findings

The fetus was a macerated, extremely

premature male infant, and his weight was 450g and crown-heel length 29cm (Fig. 1). All organs appeared expectedly premature. Subarachnoid hemorrhage was recognized at the parietal lobe of cerebrum. The placenta weighed 140g, 11.5•~11.5 Fig. 2. The maternal part of placenta cm in diameter (Fig. 2) and 3cm in (decidua basalis) thickness. Extensive infarction eminating Liquefied degenerations are seen at the from two large infarcts was seen near the central portion. umbilical cord on the cut surface of placenta. The central zones of the large infarcts demonstrated liquefied degeneration. In coloration, one infarct was reddish brown and the other was grayish-white with chocolate-color tinge (Fig. 3 and Fig. 4). In the latter lesion, microscopic examination revealed degenerated, eosin- ophilic, amorphous materials and massive fibrin deposits in the intervillous spaces (Fig. 5). Leukocytic infiltration was seen

Fig. 1. Fetus and placenta Fig. 3. Cut surfaces of the placenta Fetus is a very premature infant, and The middle three cuts reveal extensive shows severe post-mortem change with macera- infarction. tion. PLACENTAL INFARCTION 139

Fig. 4. Gross figure of the placental in- Fig. 6. Microscopic picture of the reddish farction brown colored infarct (Fig. 4) Two large infarcts are recognized. The Leukocytic infiltration and deposition of right side is a reddish brown colored infarct fibrin are seen in the intervillous spaces. and the left side is grayish white with choco- Calcifications are recognized at the periphery late-color tinge, the central zone of which of the chorionic villi. (X100, H.E.) shows liquefaction.

Fig. 5. Microscopic picture of the latter Fig. 7. Microscopic picture of the decidua infarction (Fig. 4) Thrombi are formed in the decidual small

The villi are degenerated and there are arteries. (•~100, H.E.) fibrin deposits in the intervillous spaces.

(•~100, H.E.) tion of fibrin were seen at the intervillous clinically. We have no information concer- spaces, and the chorionic villi were clearly ning the first three fetuses; thus, we are seen, with some of them showing calcifi- unable to draw any conclusions as to the cations (Fig. 6). Thrombi formation was similarity of our case to the earlier abor- seen in the decidual small arteries (Fig. 7). tions. No fetal abnormalities, such as congenital abnormalities or infections, were notable. Nor were any maternal abnor- Discussion malities, such as toxemia, incompatibility of blood groups and types, or ifections, This 31-year-old female experienced evident. Only two, large diffuse infarcts four spontaneous abortions and in each were noted primarily in the central zone case, the cause of fetal death was unknown near the umbilical cord. The necrotic areas 140 SATO, ET AL. extended from the subchorionic space to almost never the cause fetal death (Potter the basal plate. Microscopic examination and Craig, 1975). Nevertheless, Little revealed degenerated villi and fibrin depo- (1960) and Fox (1967) have stated that sition with leukocytic infiltration in the intrauterine fetal death may result from intervillous spaces. Placental infarction is extensive placental infarction involving classified into four types by Fox (1963) : more than 30% of placental tissue. Ex- true infarction, subchorionic fibrin deposi- tensive placental infarction is more com- tion, intervillous thrombosis, and perivil- mon in toxemia (preeclampsia), antepar- lous fibrin deposition. Subchorionic fibrin tum hemorrhage, and chronic renal dis- deposition is triangular, its base fused with eases than in uncomplicated pregnancies the undersurface of the chorionic plate. (Potter and Craig, 1975). Placental infarc- Microscopically, this is seen as fibrin with- tion is said to result from the interrup- out villi. Intervilous thrombosis is round tion of maternal blood flow caused by and recognized in the central or peripheral thrombosis of a spiral arteriole in the areas of the intervillous space. Microscopi- decidua (Fig. 7) or in the basal plate, cally, this shows the same picture of fibrin retroplacental hemorrhage, or hemorhage thrombus with no villi visible in the cen- into the basal plate (Fox, 1963; Potter tral area of thrombus. Perivillous fibrin and Craig, 1975). deposition is found in the peripheral area of the placenta; microscopically, fibrin deposits are seen in the intervillous spaces. References Thickened basement membrane of villi and fibrosis of the villous stroma are charac- Fox, H. (1963). White infarcts of the placenta. teristic (Fox, 1963). J. Obstet. Gynaecol. Br. Commonw. 70, 980- In this case, fetal anoxia, consequent to 991. Fox, H. (1967). The significance of placental diffuse and large true infarctions of the infarction in perinatal morbidity and mor- placenta, the cause of which are unknown, tality. Biol. Neonat. 11, 87-105. is believed to be the cause of death. Other LITTLE, W.A. (1960). Placental infarction. Ob- fetal and maternal pathology were not stet. and Gynecol. 15, 109-130. evident. POTTER, E.L. and Craig, J.M. (1975). Patho- Placental infarction is not rare, and logy of the fetus and the infant. Year Book small infarcts are common in uncomplicated Medical Publishers. Inc., Chicago, pp, 37-41. pregnancies. No relationship to intrau- RoLSCxau, J. (1978). Infarction and intervillous terine fetal death and intrauterine growth thrombosis in placenta, and their association retardation has been shown (Fox, 1967; with intrauterine growth retardation. Acta Obstet. Gynecol. Scand. (Suppl.) 72, 22-27. Rolschau, 1978). Placental infarction is