Thursday, 29 June 2017

Fetal Myocardial Infarction as Cause of Intrauterine Death


This paper describes the process by which fibrosis and calcification on the right ventricle papillary muscle –lesions associated with evolved myocardial infarction (MI)– was identified as the ultimate cause of intrauterine fetal death (FD). This is the first case described of fetal MI as a determining cause of FD in utero, with no malformative pathology or tumor present. Just a case of early neonatal death from MI due to thrombotic occlusion of the left coronary artery was found, which suggests that the event could happened during childbirth or even in utero.

The consequences of fetal death (FD) involve, primarily, a great emotional impact that affects the woman giving birth, her partner, the attending physician, and the institution assisting the event. Causes of FD have traditionally been classified into three groups: maternal, fetal and placental. Myocardial Infarction (MI), however, has never been identified as one of the causes behind FD in utero. This paper presents a case where fibrosis and calcification on the right ventricle papillary muscle –lesions directly associated with evolved MI–, were identified as the ultimate cause of intrauterine FD.

40 years old pregnant patient, P1011. Family records include father with heart disease, but no traces of coagulopathies, hypercholesterolemia or MI. She did not have any pathology or receive any added treatment. Pregnancy proceeds normally, with the last ultrasound conducted on week 32, and no ab normal findings. She did not undergo any infectious process during this time. The patient comes into the emergency room on week 33+6, reporting the absence of fetal movement during the 48 hours preceding hospital admission. The patient did not report hydrorrhea or bleeding. First examination reveals the existence of a uterine height smaller than amenorrhea, but with normal uterine tone. Cervix was closed and formed, and the fetus was in cephalic presentation. The abdominal ultrasound confirms the existence of a dead fetus, placenta on high front face and a severe oligoamnios. Blood test results were normal. Labor was induced with prostaglandins, thus ending it spontaneously. A male fetus was born with maceration signs. Fetus weighed 1800g, with Apgar score 0-0 and no apparent abnormalities. A histological study of the fetus and placenta was performed.

Male fetus with sometometry corresponding to a gestation of 33-34 weeks somatometry. Renal maturation corresponding to about 30 to 31 weeks. Less than one week maceration. No malformations, infection or neoplasia. Fibrosis and calcification of right ventricle papillary muscle (Figures 1 and 2). Extramedullar hematopoiesis inside the heart. Hyperplastic bone marrow. Scarce remains of aspiration in the lung. Placental chorionic villi with aging and ischemia signs. Retroplacental bleeding with infarction areas.

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