Final Diagnosis -- Maternal Floor Infarction

FINAL DIAGNOSIS:     MATERNAL FLOOR INFARCTION

The placenta grossly was notably pale with an edematous fetal surface. Cross sections of the placenta showed a diffuse net-like pattern of fibrinous bands. Microscopy of the placenta showed extensive fibrin deposition and obliteration of villi involving about 80% of the parenchyma. Both the gross and microscopic appearances are characteristic of the "gitterinfarkt" pattern of maternal floor infarction.

Maternal floor infarction (MFI) is an uncommon placental disease associated with recurrent third-trimester fetal loss and intrauterine growth retardation (IUGR), usually severe. The disease is characterized by extensive fibrin deposition in the intervillous spaces. The enveloped villi become atrophic and avascular. The term "infarction" is a misnomer because true placental infarcts result from arterial occlusion and ischemic necrosis of the villi. However, the functional effects of the processes are the same. Disease severity ranges from involvement of as little as one-third of the thickness of the decidua basalis to extensive involvement of the entire placental thickness. Vernof et al proposed that eddying of maternal blood in the intervillous spaces might result in this pattern of fibrin deposition. Alternatively, they propose that the histologic findings may represent a form of villous repair.

The frequency of MFI is 0.09 to 0.5 percent. In cases complicated by MFI, the rate of stillbirths is 17 to 40 percent. Growth retardation is reported in 51 to 100 percent of cases. A recurrence rate of 12 percent was reported by Andres et al, while Naeye found that pregnancies complicated by MFI were about twice as likely than controls to have been preceeded by prior abortions or stillbirths. MFI has been associated with nine reproductive failures in one woman and five consecutive failures in another.

Maternal serum alpha-fetoprotein (MSAFP) levels are occasionally elevated in MFI due to a possible disruption of the maternal-fetal interface. Mandsager et al suggest that MFI should be included in the differential diagnosis of unexplained MSAFP elevation. Ultrasonographic findings of IUGR, oligohydramnios, and a hyperechoic placenta are suggestive of possible MFI.

REFERENCES:

1. Andres RL et al. The association of maternal floor infarction of the placenta with adverse perinatal outcome. Am J Obstet Gynecol. 1990;163:935-938.
2. Gersell DJ. Chronic villitis, chronic horioamnionitis, and maternal floor infarction. Sem Diagn Pathol. 1993;10:251-266.
3. Mandsager NT et al. Maternal floor infarction of the placenta: Prenatal diagnosis and clinical significance. Obstet Gynecol. 1994;83:750-754.
4. Naeye RL. Maternal floor infarction. Hum Pathol. 1985;16:823-828.
5. Nickel RE. Maternal floor infarction: an unusual cause of intrauterine growth retardation. Am J Dis Child. 1988;142:1270-1271.
6. Vernof KK et al. Maternal floor infarction: relationship to X cells, major basic protein, and adverse perinatal outcome. Am J Obstet Gynecol. 1992;167:1355-1363.

Contributed by Ryan McCune, MD and Edward C. Klatt, MD,   Department of Pathology, University of Utah Health Sciences