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New Advances on Placental Hydrops and Related Villous Lymphatics

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New Advances on Placental Hydrops and Related Villous Lymphatics 28 Lymphology 48 (2015) 28-37 NEW ADVANCES ON PLACENTAL HYDROPS AND RELATED VILLOUS LYMPHATICS L. Roncati, G. Barbolini, T. Pusiol, F. Piscioli, A. Maiorana Department of Diagnostic and Clinical Medicine and of Public Health, Section of Pathology (LR,GB,AM), University of Modena and Reggio Emilia, Modena (MO), and Provincial Health Care Services (TP,FP), Santa Maria del Carmine Hospital, Rovereto (TN), Italy ABSTRACT search for a more suitable therapy in case of mother’s hypertension during pregnancy. Fetoplacental hydrops is the final stage of several pathological conditions in which the Keywords: placental hydrops, villous lym- placenta and umbilical cord become edematous phatics, preeclampsia, vascular endothelium, and the fetus develops an anasarcatic state podoplanin (D2-40), angiotensin-converting characterized by an excessive accumulation enzyme (ACE), Starling forces, stillbirth of extravascular fluids in at least two serous cavities of the body. It is a common histo- The first literary description of placental logical finding of stillbirth, characterized by hydrops in a twin pregnancy dates back to the appearance of markedly edematous villi, 1609 by the work of Louise Bourgeois who suggesting an increased interstitial fluid regarded it as a disease of unknown etiology accumulation. The recent improved knowledge (1). In 1892 John William Ballantyne assumed of lymphangiogenesis and the availability of its multifactorial etiology, suggesting that monoclonal antibodies selectively labeling ‘we are dealing not with a pathologic entity, lymphatic endothelium lead to the hypothesis but with a group of symptoms common to that villous edema is essentially a lymphedema several different morbid conditions’ (2). Only from defective lymphatic function following in 1946, after the identification of Rhesus inadequate villous blood circulation. Lymph- (Rh) factor, Edith Louise Potter distinguished edema is a morphologic phenotype found by immune hydrops from non-immune hydrops our research group in a 24-case series of (3). Fetoplacental hydrops is the final stage stillbirths from different morbid conditions of several pathological conditions in which such as chromosomal aberrations, congenital the placenta and umbilical cord become malformations, inherited hemoglobinopathies, edematous (hydrops placentae) and the fetus and prolonged perinatal severe anoxia. Unlike develops an anasarca state characterized by long-lived organs, the placenta is devoid of an excessive accumulation of extravascular innervation by the autonomic nervous system; fluids in at least two serous cavities of the therefore, the vascular tone regulation and body (hydrops fetalis). It may be accompanied the peripheral perfusion are modulated by by gravidic maternal complications such as the expression of the angiotensin converting preeclampsia, bleeding, and anemia, with enzyme (ACE) in the vascular endothelia. possible need for emergency cesarean section. This finding may suggest to the clinician to Grossly, a hydropic placenta, regardless of Permission granted for single print for individual use. Reproduction not permitted without permission of Journal LYMPHOLOGY. 29 the trigger causes is soft, friable, and bulky, the incidence of immune hydrops in Rh+ weighing usually more than 1000 g, with a fetuses from Rh- mothers, the form most pale cutting surface. Sometimes in the hemo- frequently found in the past (6). lytic forms a jaundiced color of the umbilical cord and superficial chorionic vessels can be Etiology seen. On microscopy, the villi appear dilated with compression of the intravillous capil- Placental hydrops is classified into laries in which nucleated red blood cells immune and non-immune hydrops. Approxi- (NRBCs) can be detected. The villous stroma mately 75% of cases are non-immune based is edematous with an increase of the cytotro- (6). Immune hydrops, also known as erythro- phoblastic shell and of Hofbauer cells. blastosis fetalis or hemolytic disease of the fetus, is caused by the transfer through the Epidemiology fetoplacental compartment of maternal antibodies directed against surface antigens Placental hydrops has an incidence of (D, C, E, Fy, Kell, ABO) of fetal red blood about 11% with a high index of fetal, peri- cells as a result of alloimmunization (previous natal, and neonatal mortality (80%) as a pregnancy, amniocentesis, abdominal trauma), function of etiology, gestational age, severity, with a consequent intravascular hemolytic and therapeutic treatments performed (4). anemia (type II hypersensitivity reaction). It correlates with a low APGAR score at birth The bone marrow compensates for this by and often intensive therapy for the neonate producing a high number of erythroblasts and is needed. The APGAR score was devised by by expanding into extramedullary sites, such Virginia Apgar in 1953 and it is based on five as spleen and liver, where marked deposits of tested parameters: Appearance (skin color), iron and consequent organ failure occur. The Pulse (heart rate), Grimace (reflex irritability), high-output heart failure related to anemia Activity (muscle tone), and Respiration and hypoproteinemia from liver failure asso- (respiratory effort) each assigned a rating ciated with an oncotic pressure decreased are from 0 to 2. The maximum achievable score responsible for the development of hydrops. is 10 (5). It is checked immediately after In 1989, Geoffrey Machin advanced a delivery with the aim to evaluate the newborn further sub-classification of non-immune adaptation to extra-uterine life, in terms of hydrops according to the root causes updated vitality and efficiency of the primary as follows: cardiovascular abnormalities, functions. More in detail, the examination is infective conditions, hematologic disorders, performed at 1, 5 and 10 minutes of the genetic defects, intrathoracic lesions, infant’s life. Infants with score less than 4 nephro-intestinal diseases, and neoplastic are in critical conditions and they require proliferations (7-10). immediate medical intervention in order to prevent longer-term neurological damage; Cardiovascular abnormalities those with a score between 4 and 6 are at risk for health in need of care, supervision, and Congestive heart failure resulting from retesting every 5 minutes; infants with score defects in electrical (tachyarrhythmias, between 7 and 10 are within a healthy normal atrioventricular blocks) or mechanical range. In the course of placental hydrops, (cardiomyopathies, premature closure of the perinatal mortality is estimated to be more foramen ovale, septal faults, endocardial than 50%, reaching 100% if genetic defects fibroelastosis, valvular insufficiencies, are concomitant to it (4). hypoplastic left heart, cardiac tumors) The introduction of maternal prophylaxis systems is the major cause of non-immune with Rho globulins has successfully reduced fetoplacental hydrops. Permission granted for single print for individual use. Reproduction not permitted without permission of Journal LYMPHOLOGY. 30 Infective conditions polycythemia. The most widely used TTTS staging system was introduced by Quintero Intrauterine infections caused by viruses et al, and it is based on ultrasound findings (Parvovirus B19, Rubella, Cytomegalovirus, (12). The TTTS Quintero staging system Herpes simplex, Hepatitis B, and Hepatitis includes five stages, ranging from mild C), bacteria (Treponema pallidum, Leptospira disease, with discordant amniotic fluid interrogans, Listeria monocytogenes) and volume, to severe disease, with demise of one protozoa (Toxoplasma gondii, Trypanosoma or both twins. More in particular, stage IV cruzi) can cause fetoplacental hydrops, refers to the presence of fetal hydrops as especially in mothers not previously exposed unfavorable prognostic factor (12). to the infective agent. Genetic defects Hematologic disorders Placental hydrops is found in fetuses Non-immune anemias and related with storage syndromes such as Gaucher hematological disorders are responsible for and Niemann-Pick, or chromosomal defect placental hydrops due to high-output heart syndromes including Down (47, +21), failure with increased serum levels of lactic Edwards (47, +18), Patau (47, +13), and acid, aldosterone and atrial natriuretic pep- Turner (45, X0). In this last case, the tide, all factors regulating the intravascular incomplete formation of the lymphatic pressure according to the Starling’s model. drainage system into the thoracic duct leads The anemias from haemoglobinopathies are to the hydropic degeneration. those most commonly associated with hydrops; more in detail, homozygous -thalassemia is Intrathoracic lesions the leading cause (86%) of fetoplacental hydrops in Southeast Asia (7). A special The intrathoracic space-occupying mention is deserved to the twin-to-twin masses, associated with a mediastinal shift, transfusion syndrome (TTS). Superficial and reduce the venous return to the heart deep vascular anastomoses are constantly resulting in the formation of hydrops with present in all monochorionic twin pregnancies; central venous hypertension. Among these however, in 15% of cases a massive shift are: congenital cystic adenomatoid malfor- of blood from a twin (donor) to another mation (CCAM), chylothorax, diaphragmatic (recipient) can occur, resulting in anemia hernia, pulmonary sequestration, pleural and polycythemia, respectively. This collection, bronchogenic cyst, hamartoma condition is known by the term twin anemia- and mediastinal tumors. polycythemia sequence (TAPS). It is a possible
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