Massive perivillous fibrin deposition

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Massive perivillous fibrin deposition
Other namesMPFD, MFD
Specialty Obstetrics, pathology
Symptoms none
Causesunknown, may be autoimmune
Risk factors previous MPFD
Diagnostic method histology of the placenta
Treatmentnone
Prognosis 33% premature birth, 31% neonatal death
Frequency0.028% of all pregnancies, 18-50% recurrence in those affected

Massive perivillous fibrin deposition (MPFD, or MFD) refers to excessive deposition of fibrous tissue around the chorionic villi of the placenta. It causes reduced growth of the foetus, and leads to miscarriage in nearly 1 in 3 pregnancies affected. There are typically no symptoms, and it is rarely detected before birth. The cause is unknown, but may be autoimmune. Diagnosis is based on the histology (cell appearance) of the placenta. There are currently no known treatments. MPFD is very rare, but recurrence is around 18% in those affected.

Contents

Signs and symptoms

There may be no symptoms of MPFD. Doppler ultrasound of the umbilical arteries may not detect reduced blood flow, particularly if a case is not severe. [1] [2]

Cause

The cause of MPFD is unknown. [3] Current theories suggest an autoimmune cause. [2] [3] It is associated with sepsis, intraventricular haemorrhage of the brain, and necrotising enterocolitis in the baby. [1] It may also be linked to maternal syphilis infection, [4] and antiphospholipid syndrome, [5] among other conditions. [6] [7]

Mechanism

MPFD is caused by deposition fibrous tissue around the chorionic villi of the placenta. [1] [3] The placenta often shows lesions upon histology and autopsy. [8] The villi become trapped, causing avascular necrosis. [1] This causes reduced substance exchange, and movement of the placenta. [1] This can cause reduce growth of the foetus, and may lead to miscarriage. [3]

Diagnosis

MPFD is diagnosed based on histological examination of the chorionic villi of the placenta. [8] Villitis of unknown etiology is distinguished by the occurrence of lymphohistiocytic infiltration in above five villi on several slides. [9] This diagnostic process is difficult, as there is great variety in appearance, and an overlap in signs with maternal floor infarction. [10]

Prognosis

MPFD always causes reduced foetal growth. [11] It causes premature birth in 33% of pregnancies, and neonatal death in 31% of pregnancies. [11]

Treatment

There are currently no widespread treatments for MPFD. [12] There is anecdotal evidence of successful use of pravastatin to reverse MPFD during pregnancy. [12]

Epidemiology

MPFD is very rare. [3] Incidence is estimated to be around 0.028%, or around 1 in 3,500 pregnancies. [11] It may account for 12% of pregnancies where foetal growth is restricted. [1] It shares symptoms with maternal floor infarction. In mothers who have already experienced it, there is a high risk of recurrence. Recurrence may be around 18%, [11] although in cases where miscarriage occur in the first trimester, it may be as high as 50%. [10]

Related Research Articles

<span class="mw-page-title-main">Placenta</span> Organ that connects the fetus to the uterine wall

The placenta is a temporary embryonic and later fetal organ that begins developing from the blastocyst shortly after implantation. It plays critical roles in facilitating nutrient, gas and waste exchange between the physically separate maternal and fetal circulations, and is an important endocrine organ, producing hormones that regulate both maternal and fetal physiology during pregnancy. The placenta connects to the fetus via the umbilical cord, and on the opposite aspect to the maternal uterus in a species-dependent manner. In humans, a thin layer of maternal decidual (endometrial) tissue comes away with the placenta when it is expelled from the uterus following birth. Placentas are a defining characteristic of placental mammals, but are also found in marsupials and some non-mammals with varying levels of development.

<span class="mw-page-title-main">Chorion</span> Outermost fetal membrane around the embryo in amniotes

The chorion is the outermost fetal membrane around the embryo in mammals, birds and reptiles (amniotes). It develops from an outer fold on the surface of the yolk sac, which lies outside the zona pellucida, known as the vitelline membrane in other animals. In insects, it is developed by the follicle cells while the egg is in the ovary. Some mollusks also have chorions as part of their eggs. For example, fragile octopus eggs have only a chorion as their envelope.

<span class="mw-page-title-main">Trophoblast</span> Early embryonic structure that gives rise to the placenta

The trophoblast is the outer layer of cells of the blastocyst. Trophoblasts are present four days after fertilization in humans. They provide nutrients to the embryo and develop into a large part of the placenta. They form during the first stage of pregnancy and are the first cells to differentiate from the fertilized egg to become extraembryonic structures that do not directly contribute to the embryo. After blastulation, the trophoblast is contiguous with the ectoderm of the embryo and is referred to as the trophectoderm. After the first differentiation, the cells in the human embryo lose their totipotency because they can no longer form a trophoblast. They become pluripotent stem cells.

<span class="mw-page-title-main">Decidua</span> Part of uterus modified in pregnancy

The decidua is the modified mucosal lining of the uterus that forms every month, in preparation for pregnancy. It is shed off each month when there is no fertilized egg to support. The decidua is under the influence of progesterone. Endometrial cells become highly characteristic. The decidua forms the maternal part of the placenta and remains for the duration of the pregnancy. After birth the decidua is shed together with the placenta.

<span class="mw-page-title-main">Syncytiotrophoblast</span> Embryonic cell of the placental surface

The syncytiotrophoblast is the epithelial covering of the highly vascular embryonic placental villi, which invades the wall of the uterus to establish nutrient circulation between the embryo and the mother. It is a multinucleate, terminally differentiated syncytium, extending to 13 cm.

<span class="mw-page-title-main">Intrauterine hypoxia</span> Medical condition when the fetus is deprived of sufficient oxygen

Intrauterine hypoxia occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction, maternal diabetes and maternal smoking. Intrauterine growth restriction may cause or be the result of hypoxia. Intrauterine hypoxia can cause cellular damage that occurs within the central nervous system. This results in an increased mortality rate, including an increased risk of sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, attention deficit hyperactivity disorder, eating disorders and cerebral palsy.

<span class="mw-page-title-main">Placenta accreta spectrum</span> Medical condition

Placenta accreta occurs when all or part of the placenta attaches abnormally to the myometrium. Three grades of abnormal placental attachment are defined according to the depth of attachment and invasion into the muscular layers of the uterus:

  1. Accreta – chorionic villi attached to the myometrium, rather than being restricted within the decidua basalis.
  2. Increta – chorionic villi invaded into the myometrium.
  3. Percreta – chorionic villi invaded through the perimetrium.
<span class="mw-page-title-main">Placentation</span> Formation and structure of the placenta

Placentation is the formation, type and structure, or arrangement of the placenta. The function of placentation is to transfer nutrients, respiratory gases, and water from maternal tissue to a growing embryo, and in some instances to remove waste from the embryo. Placentation is best known in live-bearing mammals (Theria), but also occurs in some fish, reptiles, amphibians, a diversity of invertebrates, and flowering plants. In vertebrates, placentas have evolved more than 100 times independently, with the majority of these instances occurring in squamate reptiles.

Hofbauer cells are oval eosinophilic histiocytes with granules and vacuoles found in the placenta, which are of mesenchymal origin, in mesoderm of the chorionic villi, particularly numerous in early pregnancy.

Placental insufficiency or utero-placental insufficiency is the failure of the placenta to deliver sufficient nutrients to the fetus during pregnancy, and is often a result of insufficient blood flow to the placenta. The term is also sometimes used to designate late decelerations of fetal heart rate as measured by cardiotocography or an NST, even if there is no other evidence of reduced blood flow to the placenta, normal uterine blood flow rate being 600mL/min.

<span class="mw-page-title-main">Uterine gland</span>

Uterine glands or endometrial glands are tubular glands, lined by a simple columnar epithelium, found in the functional layer of the endometrium that lines the uterus. Their appearance varies during the menstrual cycle. During the proliferative phase, uterine glands appear long due to estrogen secretion by the ovaries. During the secretory phase, the uterine glands become very coiled with wide lumens and produce a glycogen-rich secretion known as histotroph or uterine milk. This change corresponds with an increase in blood flow to spiral arteries due to increased progesterone secretion from the corpus luteum. During the pre-menstrual phase, progesterone secretion decreases as the corpus luteum degenerates, which results in decreased blood flow to the spiral arteries. The functional layer of the uterus containing the glands becomes necrotic, and eventually sloughs off during the menstrual phase of the cycle.

<span class="mw-page-title-main">Velamentous cord insertion</span> Velamentous placenta

Velamentous cord insertion is a complication of pregnancy where the umbilical cord is inserted in the fetal membranes. It is a major cause of antepartum hemorrhage that leads to loss of fetal blood and associated with high perinatal mortality. In normal pregnancies, the umbilical cord inserts into the middle of the placental mass and is completely encased by the amniotic sac. The vessels are hence normally protected by Wharton's jelly, which prevents rupture during pregnancy and labor. In velamentous cord insertion, the vessels of the umbilical cord are improperly inserted in the chorioamniotic membrane, and hence the vessels traverse between the amnion and the chorion towards the placenta. Without Wharton's jelly protecting the vessels, the exposed vessels are susceptible to compression and rupture.

<span class="mw-page-title-main">Placental disease</span> Medical condition

A placental disease is any disease, disorder, or pathology of the placenta.

<span class="mw-page-title-main">Placentitis</span> Medical condition

Placentitis is an inflammation of the placenta. The main forms of placentitis are:

<span class="mw-page-title-main">Fetal membranes</span> Amnion and chorion which surround and protect a developing fetus

The fetal membranes are the four extraembryonic membranes, associated with the developing embryo, and fetus in humans and other mammals. They are the amnion, chorion, allantois, and yolk sac. The amnion and the chorion are the chorioamniotic membranes that make up the amniotic sac which surrounds and protects the embryo. The fetal membranes are four of six accessory organs developed by the conceptus that are not part of the embryo itself, the other two are the placenta, and the umbilical cord.

<span class="mw-page-title-main">Circumvallate placenta</span> Medical condition

Circumvallate placenta is a rare condition affecting about 1-2% of pregnancies, in which the amnion and chorion fetal membranes essentially "double back" on the fetal side around the edges of the placenta. After delivery, a circumvallate placenta has a thick ring of membranes on its fetal surface. Circumvallate placenta is a placental morphological abnormality associated with increased fetal morbidity and mortality due to the restricted availability of nutrients and oxygen to the developing fetus.

<span class="mw-page-title-main">Villitis of unknown etiology</span> Medical condition

Villitis of unknown etiology (VUE), also known as chronic villitis, is a placental injury. VUE is an inflammatory condition involving the chorionic villi. VUE is a recurrent condition and can be associated with intrauterine growth restriction (IUGR). IUGR involves the poor growth of the foetus, stillbirth, miscarriage, and premature delivery. VUE recurs in about 1/3 of subsequent pregnancies.

<span class="mw-page-title-main">Placental infarction</span> Medical condition

A placental infarction results from the interruption of blood supply to a part of the placenta, causing its cells to die.

<span class="mw-page-title-main">Chorioangioma</span> Medical condition

Chorioangioma, or chorangioma, is a benign tumor of placenta. It is a hamartoma-like growth in the placenta consisting of blood vessels, and is seen in approximately 0.5 to 1% pregnancies. It is mostly diagnosed ultrasonically in the second trimester of pregnancy. Large chorioangiomas are known to cause complications in pregnancy, while the smaller ones are asymptomatic.

Breus' mole is a massive, subchorionic, tuberous hematoma formed from maternal blood in the uterus during pregnancy. It was first described by Karl Breus in 1892.

References

  1. 1 2 3 4 5 6 Spinillo, Arsenio; Gardella, Barbara; Muscettola, Giulia; Cesari, Stefania; Fiandrino, Giacomo; Tzialla, Chryssoula (November 2019). "The impact of placental massive perivillous fibrin deposition on neonatal outcome in pregnancies complicated by fetal growth restriction". Placenta. 87: 46–52. doi:10.1016/j.placenta.2019.09.007. PMID   31546153. S2CID   202747162.
  2. 1 2 Devisme, Louise; Chauvière, Claire; Franquet-Ansart, Hélène; Chudzinski, Anastasia; Stichelbout, Morgane; Houfflin-Debarge, Véronique; Subtil, Damien (April 2017). "Perinatal outcome of placental massive perivillous fibrin deposition: a case-control study". Prenatal Diagnosis. 37 (4): 323–328. doi:10.1002/pd.5013. PMID   28152557. S2CID   12908009.
  3. 1 2 3 4 5 Faye-Petersen, Ona Marie; Ernst, Linda M. (March 2013). "Maternal Floor Infarction and Massive Perivillous Fibrin Deposition". Surgical Pathology Clinics. 6 (1): 101–14. doi:10.1016/j.path.2012.10.002. PMID   26838705.
  4. ↑ Taweevisit, Mana; Thawornwong, Nutchanok; Thorner, Paul Scott (2021-01-01). "Massive Perivillous Fibrin Deposition Associated With Placental Syphilis: A Case Report". Pediatric and Developmental Pathology. 24 (1): 43–46. doi:10.1177/1093526620957523. PMID   32951526. S2CID   221826726.
  5. ↑ Sebire, Neil J; Backos, May; Goldin, Robert D.; Regan, Lesley (May 2002). "Placental massive perivillous fibrin deposition associated with antiphospholipid antibody syndrome". BJOG. 109 (5): 570–3. doi:10.1111/j.1471-0528.2002.00077.x. PMID   12066949. S2CID   33748717.
  6. ↑ Hung, Noelyn Anne; Jackson, Christopher; Nicholson, Martha; Highton, John (February 2006). "Pregnancy-related poymyositis and massive perivillous fibrin deposition in the placenta: are they pathogenetically related?". Arthritis and Rheumatism. 55 (1): 154–6. doi: 10.1002/art.21710 . PMID   16463429.
  7. ↑ Gestrich, Catherine K; Zhou, Yi Yuan; Ravishankar, Sanjita (2021-01-01). "Massive Perivillous Fibrin Deposition in Congenital Cytomegalovirus Infection: A Case Report". Pediatric and Developmental Pathology. 24 (1): 47–50. doi:10.1177/1093526620961352. PMID   33104416. S2CID   225083262.
  8. 1 2 Pathak, Sangeeta; Lees, Christoph C.; Hackett, Gerald; Jessop, Flora; Sebire, Neil J. (December 2011). "Frequency and clinical significance of placental histological lesions in an unselected population at or near term". Virchows Archiv. 459 (6): 565–72. doi:10.1007/s00428-011-1157-z. PMID   22038509. S2CID   26004303.
  9. ↑ Romero, Roberto; Whitten, Amy; Korzeniewski, Steven J.; Than, Nandor G; Chaemsaithong, Piya; Miranda, Jezid; Dong, Zhong; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn (October 2013). "Maternal Floor Infarction/Massive Perivillous Fibrin Deposition: A Manifestation of Maternal Antifetal Rejection". American Journal of Reproductive Immunology. 70 (4): 285–298. doi:10.1111/aji.12143. ISSN   1046-7408. PMC   4122226 . PMID   23905710.
  10. 1 2 Katzman, Philip J.; Genest, David R. (2002-03-01). "Maternal floor infarction and massive perivillous fibrin deposition: histological definitions, association with intrauterine fetal growth restriction, and risk of recurrence". Pediatric and Developmental Pathology. 5 (2): 159–64. doi:10.1007/s10024001-0195-y. PMID   11910510. S2CID   43397786.
  11. 1 2 3 4 Bane, Anita L.; Gillan, J. E. (March 2003). "Massive perivillous fibrinoid causing recurrent placental failure". BJOG. 110 (3): 292–5. doi:10.1016/S1470-0328(03)00919-4. PMID   12628270.
  12. 1 2 Chaiworapongsa, Tinnakorn; Romero, Roberto; Korzeniewski, Steven J.; Chaemsaithong, Piya; Hernandez-Andrade, Edgar; Segars, James H.; DeCherney, Alan H.; McCoy, M. Cathleen; Kim, Chong Jai; Yeo, Lami; Hassan, Sonia S. (March 2016). "Pravastatin to prevent recurrent fetal death in massive perivillous fibrin deposition of the placenta (MPFD)". The Journal of Maternal-Fetal & Neonatal Medicine. 29 (6): 855–62. doi:10.3109/14767058.2015.1022864. PMC   4710361 . PMID   25893545.
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