morphine and Vascular-Diseases

The authors present a case of stillbirth in which histologic examination of the placenta provides the opportunity to make a definitive diagnosis of a death due to fetal thrombotic vasculopathy (FTV). Establishing the etiology in cases of stillbirth may avoid medical malpractice litigation. The better knowledge of the cause of stillbirths also helped obstetricians to recognize factors that could have prejudiced future pregnancies.

Topics: Adult; Erythroblastosis, Fetal; Female; Forensic Pathology; Humans; Liability, Legal; Malpractice; Meconium; Placenta; Placenta Diseases; Pregnancy; Stillbirth; Vascular Diseases

A 3-day-old premature infant with meconium peritonitis, periventricular leukomalacia, and pulmonary hypertension died with respiratory insufficiency. An autopsy disclosed intravascular squamous cells in the lungs, brain, liver, pancreas, and kidneys. Numerous pulmonary capillaries and arterioles were occluded by squamous cells, accounting for pulmonary hypertension. Brain parenchyma surrounding occluded cerebral vessels showed infarct and gliosis. A mediastinal lymph node filled with squamous cells alluded to the mechanism by which these cells from the peritoneal cavity likely entered the bloodstream--namely, via diaphragmatic pores connecting with lymphatics. Thus, disseminated intravascular meconium rarely may complicate meconium peritonitis and have devastating consequences.

Topics: Embolism; Fatal Outcome; Female; Fetal Diseases; Humans; Infant, Newborn; Infant, Premature, Diseases; Meconium; Peritonitis; Pregnancy; Pregnancy Complications; Vascular Diseases

It is uncertain how often the passage of meconium in utero is a response to some event causing fetal distress as opposed to being simply the physiologic functioning of a maturing intestinal tract. The extent to which meconium may produce injury or inflammation in pulmonary and placental tissues after intrauterine exposure is also unclear. This study was a retrospective review of 123 cases, 79 stillborn and 44 liveborn less than one month of age, autopsied at The Johns Hopkins Hospital, and showing histologic evidence of intrauterine meconium exposure by aspirated meconium or meconium macrophages in placental tissues. Of 55 cases with pulmonary inflammation, 13 (24%) had fetal pneumonia, 5 (9%) had postnatal bronchopneumonia, and 37 (67%) had inflammation secondary to meconium aspiration. There was inflammation of the umbilical cord in 31 (41%) of the 75 cases with available slides, 11 (15%) had funisitis associated with chorioamnionitis and 18 (58%) were secondary to meconium exposure. There were 19 cases with focal injury of cord vessels from meconium, two of which had cord ulceration. Inflammation of the membranes and chorionic plate was present in 24 (33%) of the 72 cases where it could be assessed, and was due to chorioamnionitis in 11 (46%) and to meconium in 13 (54%). In general, meconium-related inflammations was much less severe in the membranes than in the cord. There were 67 (54%) cases with definite or probable evidence of fetal distress. In 38 (48%) stillborns no cause of fetal death in utero was identified and in 18 (41%) liveborns there was no known prenatal problem. The results support the concept that meconium passage in utero may occur either as a response to fetal distress or as a physiologic process. Inflammation in the lung and placental tissues, and vascular injury in the umbilical cord may arise secondary to in utero exposure to meconium.

Topics: Female; Fetal Death; Fetus; Humans; Infant, Newborn; Inflammation; Meconium; Meconium Aspiration Syndrome; Placenta; Placenta Diseases; Pneumonia; Pregnancy; Retrospective Studies; Umbilical Cord; Vascular Diseases

Although not proved, it is generally accepted that pulmonary vasospasm is responsible for the persistent pulmonary hypertension frequently associated with meconium aspiration. We have studied the pulmonary vasculature in 11 consecutive infants with fatal meconium aspiration, applying morphometric techniques to pulmonary arteries distended with barium gelatin before fixation. In 10 of the 11 infants, persistent pulmonary hypertension was evident clinically, with right-to-left shunting through the foramen ovale or ductus arteriosus. In all but one, severe structural abnormal muscularization of the smallest intra-acinar arteries was present. These changes must have developed before birth. In only one infant was the structure of the intra-acinar precapillary arteries virtually normal, as would be expected if vasospasm alone had caused the hypertension. The persistent pulmonary hypertension associated with fatal meconium aspiration may be the result of a structurally abnormal pulmonary microcirculation.

Topics: Female; Humans; Hypertension, Pulmonary; Infant, Newborn; Lung; Meconium; Microcirculation; Pneumonia, Aspiration; Pregnancy; Pulmonary Artery; Vascular Diseases