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Войти в исследования The American journal of forensic medicine and pathology · 2015
Histopathological Findings in Spontaneous Hematoma of the Umbilical Cord: Severe Hypoxic-Ischemic Encephalopathy in a Term Survived Newborn.
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Tonni Gabriele, Bonasoni Maria Paola, De Felice Claudio, Rossi Andrea, Tonni Silvia
Аннотация
BACKGROUND: Spontaneous hematoma of the umbilical cord is a rare, unpreventable, and dramatic event mainly due to a disruption of the vascular wall, often resulting in adverse perinatal outcome.
CASE: We describe a case of a term fetus with acute hemorrhage in the cord occurred intrapartum during spontaneous vaginal delivery. No iatrogenic factors were involved because no drugs, obstetric instruments, or procedures were applied. Umbilical hematoma probably developed in a time frame of 90 seconds, when the electronic fetal monitoring tracing detected a loss of fetal heart rate. At birth, the baby was in serious conditions with a low Apgar score (always 3 at 1, 5, and 10 minutes) and severe mixed acidosis. He was intubated, was ventilated, and underwent therapeutic hypothermia. Although all standard emergency procedures had been immediately applied, hypoxic-ischemic encephalopathy ensued within 24 hours postnatal. Placental examination revealed in the cord disruption of the elastic fibers in the vessels walls. Moreover, myofibroblasts in the Wharton's jelly appeared reduced in number and blunted, instead of their usual stellate shape. Chorioamnionitis but no funisitis was also present.Clinical follow-up of the child, aged 4 years, showed spastic tetraplegia, seizures, central deafness, and blindness.
CONCLUSIONS: Intrinsic anomalies of the cord favored vascular rupture, hematoma of the cord, and acute fetal hypoxia. Placental examination played a key role in excluding medical malpractice because hematoma of the cord was a damaging, not otherwise preventable, event.
CASE: We describe a case of a term fetus with acute hemorrhage in the cord occurred intrapartum during spontaneous vaginal delivery. No iatrogenic factors were involved because no drugs, obstetric instruments, or procedures were applied. Umbilical hematoma probably developed in a time frame of 90 seconds, when the electronic fetal monitoring tracing detected a loss of fetal heart rate. At birth, the baby was in serious conditions with a low Apgar score (always 3 at 1, 5, and 10 minutes) and severe mixed acidosis. He was intubated, was ventilated, and underwent therapeutic hypothermia. Although all standard emergency procedures had been immediately applied, hypoxic-ischemic encephalopathy ensued within 24 hours postnatal. Placental examination revealed in the cord disruption of the elastic fibers in the vessels walls. Moreover, myofibroblasts in the Wharton's jelly appeared reduced in number and blunted, instead of their usual stellate shape. Chorioamnionitis but no funisitis was also present.Clinical follow-up of the child, aged 4 years, showed spastic tetraplegia, seizures, central deafness, and blindness.
CONCLUSIONS: Intrinsic anomalies of the cord favored vascular rupture, hematoma of the cord, and acute fetal hypoxia. Placental examination played a key role in excluding medical malpractice because hematoma of the cord was a damaging, not otherwise preventable, event.