Umbilical cord hematoma is a very rare and life-threatening complication of pregnancy and is mostly seen secondary to cordcentesis. Although recent reports showed that intrauterine infection is a risk factor for the subsequent development of cerebral palsy 1, association of chorioamnionitis (CAM) and funisitis with umbilical cord hematoma has not been mentioned. A 37-year-old woman, para 2, with an uncomplicated antenatal course, at 38 weeks of gestation, developed a fever at 6:00. On admission, body temperature was 39.8°C. Vaginal examination showed rupture of the membranes. Bacteriological examination of the vaginal fluor later revealed Staphylococcus aureus. Although variable decelerations reaching near 70 beats/min were demonstrated occasionally, we confirmed the fetal well-being by the observation of both accelerations and variability (Figure 1A). The fetus suddenly developed a severe bradycardia at 10:27 and an emergency cesarean section was decided. Intrauterine death was confirmed by ultrasonography on arrival in the operating room at 10:50. Thirty-five minutes later, a stillborn female infant weighing 3,240 g was delivered through vagina. Histological examination of the umbilical cord revealed hematoma dissecting muscle layers, destroying the structure of the vein, and surrounding one of the arteries. The lesion was located close to the area of the cord insertion into the placenta. Both funisitis (grade III) and CAM (grade III) were confirmed. Fetal heart rate tracing of case 1 (A) and case 2 (B) showed sudden and persisted bradycardia. A 37-year-old woman, para 0, with an uneventful antenatal course, at 41 weeks of gestation, was admitted to our hospital for delivery. After rupture of the membranes the next day, body temperature was 38.3°C. Occasional mild variable and late decelerations with decreased variability were noted. Loss of variability was observed thereafter and was then followed by progressive bradycardia (Figure 1B). An emergency cesarean section was performed. The female infant of 2,822 g was flaccid and resuscitation was immediately started. The infant is alive with flat electroencephalography. Microscopically both funisitis (grade III) and CAM (grade III) were present. All blood vessels in the umbilical cord were encircled by hematoma. Serial sections through the hematoma revealed the destruction of the venous structure. The lesion was located close to the area of the cord insertion into the placenta. Based on the fact that infection and thrombotic lesions were sometimes found in the same placental material 2, the findings of polymorphonuclear leukocyte infiltration by histologic examination of placentas and umbilical cords in our cases strongly suggested that umbilical cord hematoma was associated with CAM and funisitis. We postulate that CAM and funisitis rendered the umbilical vessels friable partly by neutrophilic enzymes, followed by the rupture of the umbilical vein, which is the most common vessel to rupture. Then, clotting took place by the injury of vessel wall, leading to the stenosis or obstruction of the vessel. The hematoma meanwhile spread along Wharton's jelly and compressed the umbilical vessels. Umbilical artery vasospasm might be induced secondary to the cord hematoma 3. Retrospective case reviews revealed that fetal heart rate changes due to the developing hematoma included variable decelerations, late decelerations, and decrease or loss of variability 4. These changes might depend on the severity of the fetal circulatory impairment by umbilical cord hematoma. Severe and persistent bradycardia or subsequent sudden cardiac arrest is usually the final episode. These findings are not specific to umbilical hematoma, and hence, it is difficult to predict by fetal heart tracing. Although prenatal ultrasonography using color Doppler has been shown to diagnose umbilical cord hematoma 5, ultrasonography would be generally of no use without bearing umbilical cord hematoma in mind as a differential diagnosis. In conclusion, umbilical cord hematoma could be attributed to CAM and funisitis. When sudden and prolonged deceleration and subsequent fetal demise or severe asphyxia are encountered without any obvious cause, histological examination of the umbilical cord as well as the placenta should be recommended to clarify the pathogenesis and avoid a needless lawsuit.